A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.
Agents used to treat AIDS and/or stop the spread of the HIV infection. These do not include drugs used to treat symptoms or opportunistic infections associated with AIDS.
Inhibitors of reverse transcriptase (RNA-DIRECTED DNA POLYMERASE), an enzyme that synthesizes DNA on an RNA template.
A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.
A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.
A reverse transcriptase inhibitor and ZALCITABINE analog in which a sulfur atom replaces the 3' carbon of the pentose ring. It is used to treat HIV disease.
Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized. It may occur spontaneously or in association with diseases such as DIABETES MELLITUS; LEUKEMIA; or LIVER FAILURE.
Defective metabolism leading to fat maldistribution in patients infected with HIV. The etiology appears to be multifactorial and probably involves some combination of infection-induced alterations in metabolism, direct effects of antiretroviral therapy, and patient-related factors.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.
A collection of heterogenous conditions resulting from defective LIPID METABOLISM and characterized by ADIPOSE TISSUE atrophy. Often there is redistribution of body fat resulting in peripheral fat wasting and central adiposity. They include generalized, localized, congenital, and acquired lipodystrophy.
Drug regimens, for patients with HIV INFECTIONS, that aggressively suppress HIV replication. The regimens usually involve administration of three or more different drugs including a protease inhibitor.
Carbon-containing phosphonic acid compounds. Included under this heading are compounds that have carbon bound to either OXYGEN atom or the PHOSPHOROUS atom of the (P=O)O2 structure.
A potent HIV protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children.
OXAZINES with a fused BENZENE ring.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
The ability of viruses to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance phenotype may be attributed to multiple gene mutation.
Therapy with two or more separate preparations given for a combined effect.
A purine base and a fundamental unit of ADENINE NUCLEOTIDES.
The number of CD4-POSITIVE T-LYMPHOCYTES per unit volume of BLOOD. Determination requires the use of a fluorescence-activated flow cytometer.
A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.
Six-membered heterocycles containing an oxygen and a nitrogen.
The quantity of measurable virus in a body fluid. Change in viral load, measured in plasma, is sometimes used as a SURROGATE MARKER in disease progression.
A reverse transcriptase encoded by the POL GENE of HIV. It is a heterodimer of 66 kDa and 51 kDa subunits that are derived from a common precursor protein. The heterodimer also includes an RNAse H activity (RIBONUCLEASE H, HUMAN IMMUNODEFICIENCY VIRUS) that plays an essential role the viral replication process.
The ability of viruses to resist or to become tolerant to chemotherapeutic agents or antiviral agents. This resistance is acquired through gene mutation.
Nucleosides that have two hydroxy groups removed from the sugar moiety. The majority of these compounds have broad-spectrum antiretroviral activity due to their action as antimetabolites. The nucleosides are phosphorylated intracellularly to their 5'-triphosphates and act as chain-terminating inhibitors of viral reverse transcription.
Agents used to treat RETROVIRIDAE INFECTIONS.
An HIV protease inhibitor used in a fixed-dose combination with RITONAVIR. It is also an inhibitor of CYTOCHROME P-450 CYP3A.
The phosphate esters of DIDEOXYNUCLEOSIDES.
Pyrimidinones are heterocyclic organic compounds that consist of a pyrimidine ring fused with a ketone group, which have significant applications in medicinal chemistry due to their wide range of biological activities, including antibacterial, antiviral, and anticancer properties.
Drugs whose drug name is not protected by a trademark. They may be manufactured by several companies.
Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2.
A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.
A species of the genus MACACA which inhabits Malaya, Sumatra, and Borneo. It is one of the most arboreal species of Macaca. The tail is short and untwisted.
An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. It also inhibits CYTOCHROME P-450 CYP3A.
Inhibitors of HIV PROTEASE, an enzyme required for production of proteins needed for viral assembly.

A multiple drug interaction study of stavudine with agents for opportunistic infections in human immunodeficiency virus-infected patients. (1/314)

The effects of multiple opportunistic infection medications on stavudine pharmacokinetics were evaluated. Ten patients with CD4 counts of less than 200 cells/mm3 received stavudine (40 mg twice daily) in combination with one to three other drugs used to treat opportunistic infections. Serial blood samples for stavudine concentrations were collected after 1 week of therapy on each regimen and assayed for stavudine by using a validated high-pressure liquid chromatography method. Although the maximum concentration of drug in serum was significantly decreased when the drug was given in combination with three opportunistic infection medications, the area under the concentration-time curve did not significantly differ across various treatment regimens. Stavudine exposure was not significantly altered by multiple concomitant medications. Side effects were minor throughout the 3-month study period. The tolerability of stavudine, combined with its lack of drug interactions, makes it an attractive agent for use as part of a combination regimen.  (+info)

Suppression of replication of multidrug-resistant HIV type 1 variants by combinations of thymidylate synthase inhibitors with zidovudine or stavudine. (2/314)

The replication of recombinant multidrug-resistant HIV-1 clones modeled on clinically derived resistant HIV-1 strains from patients receiving long-term combination therapy with zidovudine (AZT) plus 2',3'-dideoxycytidine was found to regain sensitivity to AZT and stavudine (D4T) as a consequence of a pharmacologically induced decrease in de novo dTMP synthesis. The host-cell system used was phytohemagglutinin-stimulated peripheral blood mononuclear cells; dTMP and dTTP depletion were induced by single exposures to a low level of the thymidylate synthase inhibitor 5-fluorouracil (5-FU) or its deoxynucleoside, 2'-deoxy-5-fluorouridine. The host-cell response to the latter was biphasic: a very rapid decrease in the rate of de novo dTMP formation and, consequently, in intracellular dTTP pools, followed by slower recovery in both indices over 3 to 24 h. With the additional presence of AZT or D4T, however, replication of the multidrug-resistant HIV-1 strains remained inhibited, indicating dependence of HIV DNA chain termination by AZT-5'-monophosphate or 2',3'-didehydro-2', 3'-dideoxythymidine-5'-monophosphate in these resistant strains on simultaneous inhibition of host-cell de novo synthesis of thymidine nucleotides. No effect on viability of control (uninfected) phytohemagglutinin-stimulated/peripheral blood mononuclear cells was noted on 6-day exposures to 5-FU or 2'-deoxy-5-fluorouridine alone or in combination with AZT or D4T, even at drug levels severalfold higher than those used in the viral inhibition studies. These studies may provide useful information for the potential clinical use of AZT/5-FU or D4T/5-FU combinations for the prevention or reversal of multidrug resistance associated with long-term dideoxynucleoside combination therapy.  (+info)

The ALBI trial: a randomized controlled trial comparing stavudine plus didanosine with zidovudine plus lamivudine and a regimen alternating both combinations in previously untreated patients infected with human immunodeficiency virus. (3/314)

A total of 151 previously untreated patients infected with human immunodeficiency virus type 1 (HIV-1) with CD4 cell counts >/=200/microL and plasma HIV-1 RNA levels of 10,000-100,000 copies/mL were randomly assigned to 24 weeks of open-labeled stavudine plus didanosine (group 1), zidovudine plus lamivudine (group 2), or stavudine plus didanosine followed by zidovudine plus lamivudine (group 3). The mean decrease in HIV-1 RNA level was greater in group 1 (2.26 log10 copies/mL) than in groups 2 (1.26 log10 copies/mL) or 3 (1.58 log10 copies/mL; P<.0001). The mean increase in CD4 cell counts was greater in groups 1 (124 cells/microL) and 3 (118 cells/microL) than in group 2 (62 cells/microL; P=.02). All regimens were generally well tolerated. The combination of stavudine plus didanosine reduced plasma HIV-1 RNA concentrations and increased CD4 cell counts more effectively than did the combination of zidovudine plus lamivudine or the regimen alternating both combinations.  (+info)

Levels of human immunodeficiency virus type 1-specific cytotoxic T-lymphocyte effector and memory responses decline after suppression of viremia with highly active antiretroviral therapy. (4/314)

Therapeutic suppression of human immunodeficiency virus type 1 (HIV-1) replication may help elucidate interactions between the host cellular immune responses and HIV-1 infection. We performed a detailed longitudinal evaluation of two subjects before and after the start of highly active antiretroviral therapy (HAART). Both subjects had evidence of in vivo-activated and memory cytotoxic T-lymphocyte precursor (CTLp) activity against multiple HIV-1 gene products. After the start of therapy, both subjects had declines in the levels of in vivo-activated HIV-1-specific CTLs and had immediate increases in circulating HIV-1-specific CTL memory cells. With continued therapy, and continued suppression of viral load, levels of memory CTLps declined. HLA A*0201 peptide tetramer staining demonstrated that declining levels of in vivo-activated CTL activity were associated with a decrease in the expression of the CD38(+) activation marker. Transient increases in viral load during continued therapy were associated with increases in the levels of virus-specific CTLps in both individuals. The results were confirmed by measuring CTL responses to discrete optimal epitopes. These studies illustrate the dynamic equilibrium between the host immune response and levels of viral antigen burden and suggest that efforts to augment HIV-1-specific immune responses in subjects on HAART may decrease the incidence of virologic relapse.  (+info)

Cell-associated HIV-1 RNA in blood as indicator of virus load in lymph nodes. The Swiss HIV Cohort Study. (5/314)

We have developed sensitive assays for viremia and cell-associated human immunodeficiency virus type 1 (HIV-1) RNA and DNA to assess the predictive value of virological parameters determined in blood for virus load in lymph nodes (LNs). Eighteen patients were included; 13 received stavudine/didanosine/hydroxyurea and 5 stavudine/didanosine, and all had viremia <500 copies/mL for >3 months. At the time of LN biopsy (median, 10 months), the median viremia was 2.09 log copies/mL (range, <0.70-3.34). Cell-associated HIV-1 RNA and DNA were detectable in blood and LNs of all patients. The median cell-associated RNA and DNA were 2.16 log copies/106 cells and 2.60 log copies/106 cells in blood versus 4.31 log RNA copies/106 cells and 3.26 log DNA copies/106 cells in LNs. Regression analysis shows that, in treated patients with sustained low viremia, cell-associated RNA and DNA in blood are better predictors of virus load in LNs than viremia.  (+info)

Characterization of the activation pathway of phosphoramidate triester prodrugs of stavudine and zidovudine. (6/314)

The phosphoramidate triester prodrugs of anti-human HIV 2', 3'-dideoxynucleoside analogs (ddN) represent a convenient approach to bypass the first phosphorylation to ddN 5'-monophosphate (ddNMP), resulting in an improved formation of ddN 5'-triphosphate and, hence, higher antiviral efficacy. Although phosphoramidate derivatization markedly increases the anti-HIV activity of 2',3'-didehydro-2', 3'-dideoxythymidine (d4T) in both wild-type and thymidine kinase-deficient CEM cells, the concept is far less successful for the 3'-azido-2',3'-dideoxythymidine (AZT) triesters. We now investigated the metabolism of triester prodrugs of d4T and AZT using pure enzymes or different biological media. The efficiency of the first activation step, mediated by carboxylesterases, consists of the formation of the amino acyl ddNMP metabolite. The efficiency of this step was shown to be dependent on the amino acid, alkyl ester, and ddN moiety. Triesters that showed no conversion to the amino acyl ddNMP accumulated as the phenyl-containing intermediate and had poor, if any, anti-HIV activity. In contrast to the relative stability of the triesters in human serum, carboxylesterase-mediated cleavage of the prodrugs was found to be remarkably high in mouse serum. The subsequent conversion of the amino acyl ddNMP metabolite to ddNMP or ddN was highest in rat liver cytosolic enzyme preparations. Although L-alaninyl-d4TMP was efficiently converted to d4TMP, the main metabolite formed from L-alaninyl-AZTMP was the free nucleoside (AZT), thus explaining why d4T prodrugs, but not AZT prodrugs, retain anti-HIV activity in HIV-infected thymidine kinase-deficient cell cultures. The rat liver phosphoramidase responsible for the formation of ddNMP was shown to be distinct from creatine kinase, alkaline phosphatase, and phosphodiesterase.  (+info)

Use of recombinant viruses to assess the pattern of early human immunodeficiency virus breakthrough infection in the presence of stavudine. (7/314)

A variety of cell lines were infected with replication-defective recombinant retroviruses in the presence of stavudine (d4T). Cells which were infected despite the presence of d4T were isolated and subjected to infection with other retroviruses [replication-competent human immunodeficiency virus (HIV), replication-defective HIV or replication-defective recombinant murine retroviruses]. Each of the host cell types tested had a small subset of cells that were infected with HIV or murine retroviruses in the presence of d4T. Some of these infected cells could be infected repeatedly at high efficiency in the presence of d4T. This phenotype of 'persistent refractoriness' to the antiviral effects of d4T could be overcome by the addition of 5-fluoro-2-deoxyuridine (floxuridine) to d4T. The d4T-floxuridine combination also had potent antiretroviral effects in primary blood mononuclear cells.  (+info)

Intracellular metabolism of CycloSaligenyl 3'-azido-2', 3'-dideoxythymidine monophosphate, a prodrug of 3'-azido-2', 3'-dideoxythymidine (zidovudine). (8/314)

The administration of CycloSaligenyl 3'-azido-2',3'-dideoxythymidine monophosphate (CycloSal-AZTMP) to CEM cells resulted in a concentration- and time-dependent conversion to the 5'-monophosphate (AZTMP), 5'-diphosphate (AZTDP), and 5'-triphosphate (AZTTP) derivatives. High ratios of AZTMP/AZTTP were found in the CEM cell cultures treated with CycloSal-AZTMP. The intracellular T(1/2) of AZTTP in CEM cell cultures treated with either AZT and CycloSal-AZTMP was approximately 3 h. A variety of human T- and B-lymphocyte cell lines efficiently converted the prodrug to the AZT metabolites, whereas peripheral blood lymphocytes and primary monocyte/macrophages showed at least 10-fold lower metabolic conversion of the prodrug. CycloSal-AZTMP failed to generate marked levels of AZT metabolites in thymidine kinase-deficient CEM/TK(-) cells, an observation that is in agreement with the substantial loss of antiviral activity of CycloSal-AZTMP in CEM/TK(-) cells. The inability of CycloSal-AZTMP to generate AZTMP in CEM/TK(-) cells is presumably due to a relatively high hydrolysis rate of AZTMP to the parent nucleoside AZT, combined with the inability of CEM/TK(-) cells to phosphorylate AZT to AZTMP through the cytosolic salvage enzyme thymidine kinase.  (+info)

Stavudine is an antiviral medication used to treat HIV (human immunodeficiency virus) infections. It works by blocking the action of reverse transcriptase, an enzyme that the virus needs to multiply. By preventing the multiplication of the virus, Stavudine helps reduce the amount of HIV in the body and slows down the progression of the disease.

Stavudine is often prescribed in combination with other antiretroviral drugs as part of a highly active antiretroviral therapy (HAART) regimen. It is available in oral form, typically taken twice daily, and is usually prescribed at a dose of 40 milligrams per dose for adults.

It's important to note that Stavudine can cause serious side effects, including peripheral neuropathy (nerve damage that causes pain, numbness, or tingling in the hands and feet), pancreatitis (inflammation of the pancreas), and lipoatrophy (loss of fat tissue under the skin). As a result, it is generally only prescribed when other antiretroviral drugs are not effective or tolerated.

If you have any questions about Stavudine or your HIV treatment regimen, be sure to talk with your healthcare provider.

Anti-HIV agents are a class of medications specifically designed to treat HIV (Human Immunodeficiency Virus) infection. These drugs work by interfering with various stages of the HIV replication cycle, preventing the virus from infecting and killing CD4+ T cells, which are crucial for maintaining a healthy immune system.

There are several classes of anti-HIV agents, including:

1. Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs): These drugs act as faulty building blocks that the virus incorporates into its genetic material, causing the replication process to halt. Examples include zidovudine (AZT), lamivudine (3TC), and tenofovir.
2. Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs): These medications bind directly to the reverse transcriptase enzyme, altering its shape and preventing it from functioning properly. Examples include efavirenz, nevirapine, and rilpivirine.
3. Protease Inhibitors (PIs): These drugs target the protease enzyme, which is responsible for cleaving viral polyproteins into functional components. By inhibiting this enzyme, PIs prevent the formation of mature, infectious virus particles. Examples include atazanavir, darunavir, and lopinavir.
4. Integrase Strand Transfer Inhibitors (INSTIs): These medications block the integrase enzyme, which is responsible for inserting the viral genetic material into the host cell's DNA. By inhibiting this step, INSTIs prevent the virus from establishing a permanent infection within the host cell. Examples include raltegravir, dolutegravir, and bictegravir.
5. Fusion/Entry Inhibitors: These drugs target different steps of the viral entry process, preventing HIV from infecting CD4+ T cells. Examples include enfuvirtide (T-20), maraviroc, and ibalizumab.
6. Post-Attachment Inhibitors: This class of medications prevents the virus from attaching to the host cell's receptors, thereby inhibiting infection. Currently, there is only one approved post-attachment inhibitor, fostemsavir.

Combination therapy using multiple classes of antiretroviral drugs has been shown to effectively suppress viral replication and improve clinical outcomes in people living with HIV. Regular adherence to the prescribed treatment regimen is crucial for maintaining an undetectable viral load and reducing the risk of transmission.

Reverse Transcriptase Inhibitors (RTIs) are a class of antiretroviral drugs that are primarily used in the treatment and management of HIV (Human Immunodeficiency Virus) infection. They work by inhibiting the reverse transcriptase enzyme, which is essential for the replication of HIV.

HIV is a retrovirus, meaning it has an RNA genome and uses a unique enzyme called reverse transcriptase to convert its RNA into DNA. This process is necessary for the virus to integrate into the host cell's genome and replicate. Reverse Transcriptase Inhibitors interfere with this process by binding to the reverse transcriptase enzyme, preventing it from converting the viral RNA into DNA.

RTIs can be further divided into two categories: nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs). NRTIs are analogs of the building blocks of DNA, which get incorporated into the growing DNA chain during replication, causing termination of the chain. NNRTIs bind directly to the reverse transcriptase enzyme, causing a conformational change that prevents it from functioning.

By inhibiting the reverse transcriptase enzyme, RTIs can prevent the virus from replicating and reduce the viral load in an infected individual, thereby slowing down the progression of HIV infection and AIDS (Acquired Immunodeficiency Syndrome).

Zidovudine is defined as an antiretroviral medication used to prevent and treat HIV/AIDS. It is a reverse transcriptase inhibitor (NRTI) that works by blocking the action of the reverse transcriptase enzyme, thereby preventing the virus from replicating in human cells.

Zidovudine is often used in combination with other antiretroviral drugs as part of highly active antiretroviral therapy (HAART) to manage HIV infection and reduce the risk of transmission. It is also used to prevent mother-to-child transmission of HIV during pregnancy, labor, delivery, and breastfeeding.

The most common side effects of zidovudine include headache, nausea, vomiting, and muscle pain. Prolonged use of zidovudine can lead to serious side effects such as anemia, neutropenia, and lactic acidosis. Therefore, regular monitoring of blood counts and liver function tests is necessary during treatment with this medication.

Didanosine is a medication used to treat HIV (human immunodeficiency virus) infection. It is an antiretroviral drug, specifically a nucleoside reverse transcriptase inhibitor (NRTI), that works by interfering with the replication of the virus in the body. Didanosine is often used in combination with other antiretroviral drugs as part of highly active antiretroviral therapy (HAART) to help control HIV infection and reduce the risk of HIV-related illnesses.

The medical definition of 'Didanosine' is:

A synthetic nucleoside analogue that inhibits the reverse transcriptase activity of the human immunodeficiency virus (HIV). It is converted in vivo to the active metabolite dideoxyadenosine triphosphate, which competitively inhibits HIV DNA polymerase and has antiviral properties. The drug is used in the treatment of HIV infection and AIDS.

Lamivudine is an antiretroviral medication used in the treatment and management of HIV (Human Immunodeficiency Virus) infection and HBV (Hepatitis B Virus) infection. It is a nucleoside reverse transcriptase inhibitor (NRTI), which means it works by blocking the action of the reverse transcriptase enzyme that the viruses need to multiply. By doing this, Lamivudine helps to reduce the amount of the virus in the body, which in turn helps to slow down or prevent the damage that the virus can cause to the immune system and improve the patient's quality of life.

The medical definition of Lamivudine is: "A synthetic nucleoside analogue with activity against both HIV-1 and HBV. It is used in the treatment of HIV infection and AIDS, as well as chronic hepatitis B."

Lactic acidosis is a medical condition characterized by an excess accumulation of lactic acid in the body. Lactic acid is a byproduct produced in the muscles and other tissues during periods of low oxygen supply or increased energy demand. Under normal circumstances, lactic acid is quickly metabolized and cleared from the body. However, when the production of lactic acid exceeds its clearance, it can lead to a state of acidosis, where the pH of the blood becomes too acidic.

Lactic acidosis can be caused by several factors, including:

* Prolonged exercise or strenuous physical activity
* Severe illness or infection
* Certain medications, such as metformin and isoniazid
* Alcoholism
* Hypoxia (low oxygen levels) due to lung disease, heart failure, or anemia
* Inherited metabolic disorders that affect the body's ability to metabolize lactic acid

Symptoms of lactic acidosis may include rapid breathing, fatigue, muscle weakness, nausea, vomiting, and abdominal pain. Severe cases can lead to coma, organ failure, and even death. Treatment typically involves addressing the underlying cause of the condition and providing supportive care, such as administering intravenous fluids and bicarbonate to help restore normal pH levels.

HIV-Associated Lipodystrophy Syndrome is a term used to describe a range of body shape changes and metabolic abnormalities that can occur in some individuals receiving long-term combination antiretroviral therapy (cART) for HIV infection. The syndrome is characterized by the abnormal distribution of fat, including:

1. Lipoatrophy: Loss of subcutaneous fat from the face, limbs, and buttocks, leading to a gaunt appearance.
2. Lipohypertrophy: Accumulation of fat in the abdomen, breasts, and dorsocervical region (buffalo hump), resulting in an altered body shape.
3. Metabolic abnormalities: Insulin resistance, hyperlipidemia, and lactic acidosis, which can increase the risk of developing cardiovascular disease and diabetes mellitus.

The exact pathogenesis of HIV-Associated Lipodystrophy Syndrome is not fully understood, but it is believed to be related to a combination of factors, including the direct effects of HIV infection on adipose tissue, mitochondrial toxicity caused by certain antiretroviral medications, and chronic inflammation. The syndrome can have significant psychological and social consequences for affected individuals, and management typically involves a multidisciplinary approach that includes switching to alternative antiretroviral regimens, addressing metabolic abnormalities, and providing cosmetic interventions as needed.

HIV (Human Immunodeficiency Virus) infection is a viral illness that progressively attacks and weakens the immune system, making individuals more susceptible to other infections and diseases. The virus primarily infects CD4+ T cells, a type of white blood cell essential for fighting off infections. Over time, as the number of these immune cells declines, the body becomes increasingly vulnerable to opportunistic infections and cancers.

HIV infection has three stages:

1. Acute HIV infection: This is the initial stage that occurs within 2-4 weeks after exposure to the virus. During this period, individuals may experience flu-like symptoms such as fever, fatigue, rash, swollen glands, and muscle aches. The virus replicates rapidly, and the viral load in the body is very high.
2. Chronic HIV infection (Clinical latency): This stage follows the acute infection and can last several years if left untreated. Although individuals may not show any symptoms during this phase, the virus continues to replicate at low levels, and the immune system gradually weakens. The viral load remains relatively stable, but the number of CD4+ T cells declines over time.
3. AIDS (Acquired Immunodeficiency Syndrome): This is the most advanced stage of HIV infection, characterized by a severely damaged immune system and numerous opportunistic infections or cancers. At this stage, the CD4+ T cell count drops below 200 cells/mm3 of blood.

It's important to note that with proper antiretroviral therapy (ART), individuals with HIV infection can effectively manage the virus, maintain a healthy immune system, and significantly reduce the risk of transmission to others. Early diagnosis and treatment are crucial for improving long-term health outcomes and reducing the spread of HIV.

Nevirapine is defined as an antiretroviral medication used to treat and prevent HIV/AIDS. It is a non-nucleoside reverse transcriptase inhibitor (NNRTI) that works by binding to and disrupting the activity of the reverse transcriptase enzyme, which is necessary for HIV replication. By blocking this enzyme, Nevirapine prevents the virus from multiplying in the body, reducing the amount of virus in the bloodstream and slowing down the progression of the disease.

Nevirapine is often used in combination with other antiretroviral drugs as part of a highly active antiretroviral therapy (HAART) regimen. It is available in tablet form and is usually taken once or twice daily, depending on the dosage prescribed by a healthcare provider. Common side effects of Nevirapine include rash, nausea, headache, and fatigue. In rare cases, Nevirapine can cause severe liver toxicity, so patients should be closely monitored for signs of liver damage during treatment.

Lipodystrophy is a medical condition characterized by abnormal distribution or absence of fat (adipose tissue) in the body. It can lead to metabolic complications such as insulin resistance, diabetes mellitus, high levels of fats in the blood (dyslipidemia), and liver disease. There are different types of lipodystrophy, including congenital generalized lipodystrophy, acquired generalized lipodystrophy, and partial lipodystrophy, which can affect different parts of the body and have varying symptoms and causes.

Antiretroviral Therapy, Highly Active (HAART) is a medical treatment regimen used to manage HIV infection. It involves the combination of three or more antiretroviral drugs from at least two different classes, aiming to maximally suppress viral replication and prevent the development of drug resistance. The goal of HAART is to reduce the amount of HIV in the body to undetectable levels, preserve immune function, and improve quality of life for people living with HIV. Commonly used antiretroviral classes include nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), integrase strand transfer inhibitors (INSTIs), and fusion inhibitors.

Organophosphonates are a class of organic compounds characterized by the presence of a carbon-phosphorus bond. They contain a phosphonic acid group, which consists of a phosphorus atom bonded to four oxygen or nitrogen atoms, with one of those bonds being replaced by a carbon atom.

In a medical context, organophosphonates are commonly used as radiopharmaceuticals in diagnostic nuclear medicine procedures, such as bone scans. These compounds have the ability to bind to hydroxyapatite, the mineral component of bones, and can be labeled with radioactive isotopes for imaging purposes. They may also be used in therapeutic settings, including as treatments for conditions such as tumor-induced hypercalcemia and Paget's disease of bone.

It is important to note that organophosphonates are distinct from organophosphates, another class of compounds that contain a phosphorus atom bonded to three oxygen or sulfur atoms and one carbon atom. Organophosphates have been widely used as pesticides and chemical warfare agents, and can pose significant health risks due to their toxicity.

Nelfinavir is a medication that belongs to a class of antiretroviral drugs called protease inhibitors. It is used in combination with other antiretroviral agents for the treatment of human immunodeficiency virus (HIV) infection and acquired immune deficiency syndrome (AIDS). Nelfinavir works by blocking the activity of HIV protease, an enzyme that is necessary for the replication of the virus. By inhibiting this enzyme, nelfinavir prevents the virus from multiplying and thus slows down the progression of the disease.

Here's a medical definition of Nelfinavir:

"Nelfinavir mesylate is a synthetic peptidomimetic inhibitor of the HIV-1 protease, an enzyme essential for the processing of viral gag and gag-pol polyproteins, reverse transcriptase, and integrase. Nelfinavir is used in combination with other antiretroviral agents for the treatment of HIV infection and AIDS."

It's important to note that nelfinavir is not a cure for HIV or AIDS, but it can help manage the disease by reducing the amount of virus in the body and improving the immune system function. As with any medication, nelfinavir has potential side effects and risks, so it should be taken under the guidance and supervision of a healthcare provider.

Benzoxazines are a class of heterocyclic organic compounds that contain a benzene fused to an oxazine ring. They are known for their diverse chemical and pharmacological properties, including anti-inflammatory, antimicrobial, and antitumor activities. Some benzoxazines also exhibit potential as building blocks in the synthesis of pharmaceuticals and materials. However, it is important to note that specific medical definitions for individual compounds within this class may vary depending on their unique structures and properties.

HIV-1 (Human Immunodeficiency Virus type 1) is a species of the retrovirus genus that causes acquired immunodeficiency syndrome (AIDS). It is primarily transmitted through sexual contact, exposure to infected blood or blood products, and from mother to child during pregnancy, childbirth, or breastfeeding. HIV-1 infects vital cells in the human immune system, such as CD4+ T cells, macrophages, and dendritic cells, leading to a decline in their numbers and weakening of the immune response over time. This results in the individual becoming susceptible to various opportunistic infections and cancers that ultimately cause death if left untreated. HIV-1 is the most prevalent form of HIV worldwide and has been identified as the causative agent of the global AIDS pandemic.

Multiple drug resistance (MDR) in viruses refers to the ability of a virus to resist or inhibit the effects of multiple antiviral agents. This occurs when a virus mutates and develops mechanisms that prevent antiviral drugs from effectively binding to their target sites, rendering the drugs unable to suppress viral replication.

In the context of virology, "multiple" typically means resistance to at least three or more classes of antiviral drugs. This is a significant concern in the management of viral infections such as HIV, HCV, and influenza, where MDR can lead to reduced treatment options, increased risk of disease progression, and potential transmission of resistant strains. Regular monitoring and appropriate use of antiviral agents are crucial for preventing and managing multiple drug resistance in viruses.

Combination drug therapy is a treatment approach that involves the use of multiple medications with different mechanisms of action to achieve better therapeutic outcomes. This approach is often used in the management of complex medical conditions such as cancer, HIV/AIDS, and cardiovascular diseases. The goal of combination drug therapy is to improve efficacy, reduce the risk of drug resistance, decrease the likelihood of adverse effects, and enhance the overall quality of life for patients.

In combining drugs, healthcare providers aim to target various pathways involved in the disease process, which may help to:

1. Increase the effectiveness of treatment by attacking the disease from multiple angles.
2. Decrease the dosage of individual medications, reducing the risk and severity of side effects.
3. Slow down or prevent the development of drug resistance, a common problem in chronic diseases like HIV/AIDS and cancer.
4. Improve patient compliance by simplifying dosing schedules and reducing pill burden.

Examples of combination drug therapy include:

1. Antiretroviral therapy (ART) for HIV treatment, which typically involves three or more drugs from different classes to suppress viral replication and prevent the development of drug resistance.
2. Chemotherapy regimens for cancer treatment, where multiple cytotoxic agents are used to target various stages of the cell cycle and reduce the likelihood of tumor cells developing resistance.
3. Cardiovascular disease management, which may involve combining medications such as angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, diuretics, and statins to control blood pressure, heart rate, fluid balance, and cholesterol levels.
4. Treatment of tuberculosis, which often involves a combination of several antibiotics to target different aspects of the bacterial life cycle and prevent the development of drug-resistant strains.

When prescribing combination drug therapy, healthcare providers must carefully consider factors such as potential drug interactions, dosing schedules, adverse effects, and contraindications to ensure safe and effective treatment. Regular monitoring of patients is essential to assess treatment response, manage side effects, and adjust the treatment plan as needed.

Adenine is a purine nucleotide base that is a fundamental component of DNA and RNA, the genetic material of living organisms. In DNA, adenine pairs with thymine via double hydrogen bonds, while in RNA, it pairs with uracil. Adenine is essential for the structure and function of nucleic acids, as well as for energy transfer reactions in cells through its role in the formation of adenosine triphosphate (ATP), the primary energy currency of the cell.

A CD4 lymphocyte count is a laboratory test that measures the number of CD4 T-cells (also known as CD4+ T-cells or helper T-cells) in a sample of blood. CD4 cells are a type of white blood cell that plays a crucial role in the body's immune response, particularly in fighting off infections caused by viruses and other pathogens.

CD4 cells express a protein on their surface called the CD4 receptor, which is used by human immunodeficiency virus (HIV) to infect and destroy these cells. As a result, people with HIV infection or AIDS often have low CD4 lymphocyte counts, which can make them more susceptible to opportunistic infections and other complications.

A normal CD4 lymphocyte count ranges from 500 to 1,200 cells per cubic millimeter of blood (cells/mm3) in healthy adults. A lower than normal CD4 count is often used as a marker for the progression of HIV infection and the development of AIDS. CD4 counts are typically monitored over time to assess the effectiveness of antiretroviral therapy (ART) and to guide clinical decision-making regarding the need for additional interventions, such as prophylaxis against opportunistic infections.

Indinavir is an antiretroviral medication used in the treatment and management of HIV (Human Immunodeficiency Virus) infection. It belongs to a class of drugs known as protease inhibitors, which work by blocking the action of protease enzymes that are necessary for the HIV virus to replicate. By inhibiting this process, indinavir helps prevent the spread of HIV in the body and reduces the risk of developing AIDS (Acquired Immunodeficiency Syndrome).

Indinavir is often prescribed as part of a combination therapy regimen with other antiretroviral drugs. It is available in capsule form and is typically taken several times a day, usually on an empty stomach. As with all medications, indinavir can have side effects, which may include nausea, diarrhea, headache, and changes in liver function. Regular monitoring of blood tests is necessary to ensure that the drug is working effectively and not causing any harmful side effects.

It's important to note that while antiretroviral therapy can help manage HIV infection and improve quality of life, it does not cure the disease. Therefore, it is essential for individuals with HIV to continue taking their medications as prescribed and to follow up regularly with their healthcare provider.

Oxazines are heterocyclic organic compounds that contain a six-membered ring with one nitrogen atom, one oxygen atom, and four carbon atoms. The structure of oxazine is similar to benzene, but with one methine group (=CH−) replaced by a nitrogen atom and another methine group replaced by an oxygen atom.

Oxazines have important applications in the pharmaceutical industry as they are used in the synthesis of various drugs, including anti-inflammatory, antiviral, and anticancer agents. However, oxazines themselves do not have a specific medical definition, as they refer to a class of chemical compounds rather than a medical condition or treatment.

Viral load refers to the amount or quantity of virus (like HIV, Hepatitis C, SARS-CoV-2) present in an individual's blood or bodily fluids. It is often expressed as the number of virus copies per milliliter of blood or fluid. Monitoring viral load is important in managing and treating certain viral infections, as a higher viral load may indicate increased infectivity, disease progression, or response to treatment.

HIV Reverse Transcriptase is an enzyme that is encoded by the HIV-1 and HIV-2 viruses. It plays a crucial role in the replication cycle of the human immunodeficiency virus (HIV), which causes AIDS.

Reverse transcriptase is responsible for transcribing the viral RNA genome into DNA, a process known as reverse transcription. This allows the viral genetic material to integrate into the host cell's DNA and replicate along with it, leading to the production of new virus particles.

The enzyme has three distinct activities: a polymerase activity that synthesizes DNA using RNA as a template, an RNase H activity that degrades the RNA template during reverse transcription, and a DNA-dependent DNA polymerase activity that synthesizes DNA using a DNA template.

Reverse transcriptase inhibitors are a class of antiretroviral drugs used to treat HIV infection. They work by binding to and inhibiting the activity of the reverse transcriptase enzyme, thereby preventing the virus from replicating.

Drug resistance, viral, refers to the ability of a virus to continue replicating in the presence of antiviral drugs that are designed to inhibit or stop its growth. This occurs when the virus mutates and changes its genetic makeup in such a way that the drug can no longer effectively bind to and inhibit the function of its target protein, allowing the virus to continue infecting host cells and causing disease.

Viral drug resistance can develop due to several factors, including:

1. Mutations in the viral genome that alter the structure or function of the drug's target protein.
2. Changes in the expression levels or location of the drug's target protein within the virus-infected cell.
3. Activation of alternative pathways that allow the virus to replicate despite the presence of the drug.
4. Increased efflux of the drug from the virus-infected cell, reducing its intracellular concentration and effectiveness.

Viral drug resistance is a significant concern in the treatment of viral infections such as HIV, hepatitis B and C, herpes simplex virus, and influenza. It can lead to reduced treatment efficacy, increased risk of treatment failure, and the need for more toxic or expensive drugs. Therefore, it is essential to monitor viral drug resistance during treatment and adjust therapy accordingly to ensure optimal outcomes.

Dideoxynucleosides are a type of modified nucleoside used in the treatment of certain viral infections, such as HIV and HBV. These compounds lack a hydroxyl group (-OH) at the 3'-carbon position of the sugar moiety, which prevents them from being further metabolized into DNA.

When incorporated into a growing DNA chain during reverse transcription, dideoxynucleosides act as chain terminators, inhibiting viral replication. Common examples of dideoxynucleosides include zidovudine (AZT), didanosine (ddI), stavudine (d4T), and lamivudine (3TC). These drugs are often used in combination with other antiretroviral agents to form highly active antiretroviral therapy (HAART) regimens for the treatment of HIV infection.

Anti-retroviral agents are a class of drugs used to treat and prevent infections caused by retroviruses, most commonly the human immunodeficiency virus (HIV). These medications work by interfering with the replication process of the retrovirus, thereby preventing it from infecting and destroying immune cells.

There are several different classes of anti-retroviral agents, including:

1. Nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) - These drugs block the action of the reverse transcriptase enzyme, which is necessary for the retrovirus to convert its RNA into DNA.
2. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) - These drugs bind directly to the reverse transcriptase enzyme and alter its shape, preventing it from functioning properly.
3. Protease inhibitors (PIs) - These drugs block the action of the protease enzyme, which is necessary for the retrovirus to assemble new viral particles.
4. Integrase inhibitors (INIs) - These drugs block the action of the integrase enzyme, which is necessary for the retrovirus to integrate its DNA into the host cell's genome.
5. Fusion inhibitors - These drugs prevent the retrovirus from entering host cells by blocking the fusion of the viral and host cell membranes.
6. Entry inhibitors - These drugs prevent the retrovirus from attaching to and entering host cells.

Anti-retroviral therapy (ART) typically involves a combination of at least three different anti-retroviral agents from two or more classes, in order to effectively suppress viral replication and prevent drug resistance. Regular monitoring of viral load and CD4+ T cell counts is necessary to ensure the effectiveness of ART and make any necessary adjustments to the treatment regimen.

Lopinavir is an antiretroviral medication used in the treatment and management of HIV (Human Immunodeficiency Virus) infection. It is a protease inhibitor, which works by blocking the action of protease, an enzyme that the virus needs to multiply. Lopinavir is often prescribed in combination with other antiretroviral drugs as part of highly active antiretroviral therapy (HAART). The medication is available under the brand name Kaletra, which is a fixed-dose combination of lopinavir and ritonavir.

It's important to note that while lopinavir can help manage HIV infection and reduce the risk of transmission, it does not cure the disease. Regular adherence to the medication regimen is necessary to maintain its effectiveness and prevent the development of drug-resistant strains of the virus.

Dideoxynucleotides are analogs of nucleotides, which are the building blocks of DNA and RNA. In a nucleotide, there is a sugar molecule (deoxyribose in DNA and ribose in RNA) attached to a phosphate group and one of four nitrogenous bases (adenine, guanine, cytosine, or thymine in DNA; adenine, guanine, cytosine, or uracil in RNA).

In a dideoxynucleotide, there are two fewer oxygen molecules on the sugar component. Specifically, instead of having a hydroxyl group (-OH) at both the 2' and 3' carbons of the sugar, a dideoxynucleotide has a hydrogen atom (-H) at the 3' carbon and a hydroxyl or another group at the 2' carbon.

Dideoxynucleotides are used in scientific research and medical diagnostics, most notably in the Sanger method of DNA sequencing. In this process, DNA polymerase adds nucleotides to a single-stranded DNA template during replication. When a dideoxynucleotide is incorporated into the growing DNA chain, it acts as a terminator because there is no 3' hydroxyl group for the next nucleotide to be added. By running multiple reactions with different dideoxynucleotides and comparing the lengths of the resulting DNA fragments, researchers can determine the sequence of the template DNA.

Dideoxynucleotides are also used as antiretroviral drugs in the treatment of HIV infection. They inhibit the reverse transcriptase enzyme that HIV uses to convert its RNA genome into DNA, thus preventing the virus from replicating. Examples of dideoxynucleoside analog reverse transcriptase inhibitors (ddNRTIs) include zidovudine (AZT), didanosine (ddI), stavudine (d4T), and lamivudine (3TC).

Pyrimidinones are a class of heterocyclic organic compounds that contain a pyrimidine ring fused with a ketone group. The basic structure of a pyrimidinone consists of two nitrogen atoms and four carbon atoms in a six-membered ring, with a carbonyl (C=O) group attached to one of the carbon atoms.

In a medical context, pyrimidinones are important because many naturally occurring and synthetic compounds that contain this structure have been found to have biological activity. For example, some pyrimidinones have antiviral, antibacterial, or anticancer properties, making them useful in the development of new drugs for various medical conditions.

One well-known drug that contains a pyrimidinone ring is the antiviral medication Ribavirin, which is used to treat hepatitis C and certain viral hemorrhagic fevers. Other pyrimidinones are being studied for their potential therapeutic benefits in areas such as cancer therapy, neuroprotection, and inflammation.

A generic drug is a medication that contains the same active ingredients as an originally marketed brand-name drug, known as its "innovator" or "reference listed" drug. The active ingredient is the component of the drug that is responsible for its therapeutic effect. Generic drugs are required to have the same quality, strength, purity, and stability as their brand-name counterparts. They must also meet the same rigorous Food and Drug Administration (FDA) standards regarding safety, effectiveness, and manufacturing.

Generic drugs are typically less expensive than their brand-name equivalents because generic manufacturers do not have to repeat the costly clinical trials that were required for the innovator drug. Instead, they demonstrate through bioequivalence studies that their product is therapeutically equivalent to the reference listed drug. This means that the generic drug delivers the same amount of active ingredient into a patient's bloodstream in the same timeframe as the brand-name drug.

In summary, generic drugs are copies of brand-name drugs with the same active ingredients, dosage forms, strengths, routes of administration, and intended uses. They must meet FDA regulations for safety, efficacy, and manufacturing standards, ensuring that they provide patients with the same therapeutic benefits as their brand-name counterparts at a more affordable price.

HIV (Human Immunodeficiency Virus) is a species of lentivirus (a subgroup of retrovirus) that causes HIV infection and over time, HIV infection can lead to AIDS (Acquired Immunodeficiency Syndrome). This virus attacks the immune system, specifically the CD4 cells, also known as T cells, which are a type of white blood cell that helps coordinate the body's immune response. As HIV destroys these cells, the body becomes more vulnerable to other infections and diseases. It is primarily spread through bodily fluids like blood, semen, vaginal fluids, and breast milk.

It's important to note that while there is no cure for HIV, with proper medical care, HIV can be controlled. Treatment for HIV is called antiretroviral therapy (ART). If taken as prescribed, this medicine reduces the amount of HIV in the body to a very low level, which keeps the immune system working and prevents illness. This treatment also greatly reduces the risk of transmission.

Zalcitabine (also known as ddC) is an antiretroviral medication used in the treatment of HIV infection. It belongs to a class of drugs called nucleoside reverse transcriptase inhibitors (NRTIs). Zalcitabine works by interfering with the replication of the virus, thus slowing down the progression of the disease.

The medical definition of Zalcitabine is: "A synthetic pyrimidine nucleoside analogue used as an antiretroviral agent in the treatment of HIV infection. It is converted to its active 5'-triphosphate form, which inhibits the activity of reverse transcriptase and results in chain termination."

It is important to note that Zalcitabine has been largely replaced by other antiretroviral drugs due to its significant side effects and the development of better treatment options.

"Macaca nemestrina," also known as the pig-tailed macaque, is not a medical term but a species name in biology. It refers to a specific species of monkey that is native to Southeast Asia. The pig-tailed macaque is a medium-sized monkey with a reddish-brown fur and a distinctive tail that resembles a pig's tail. They are omnivorous and live in social groups that can range from a few individuals to several hundred.

While "Macaca nemestrina" may not have a direct medical definition, these monkeys have been used as models in biomedical research due to their close genetic relationship with humans. Some studies involving pig-tailed macaques have contributed to our understanding of various human diseases and conditions, such as infectious diseases, neurological disorders, and reproductive health. However, it is important to note that the use of animals in research remains a controversial topic, and ethical considerations must be taken into account when conducting such studies.

Ritonavir is an antiretroviral medication used in the treatment and prevention of HIV/AIDS. It is a protease inhibitor, which works by blocking the action of protease, an enzyme that the virus needs to multiply. By doing this, Ritonavir helps to reduce the amount of HIV in the body, keeping it at a low level and preventing the disease from progressing.

Ritonavir is often used in combination with other antiretroviral drugs as part of highly active antiretroviral therapy (HAART). It is also sometimes used at lower doses to boost the levels of other protease inhibitors in the body, a practice known as "pharmacologic boosting."

It's important to note that Ritonavir does not cure HIV/AIDS, but it can help people with HIV live longer, healthier lives. As with all medications, Ritonavir can have side effects, and it may interact with other drugs, so it's important to take it exactly as prescribed by a healthcare provider.

HIV Protease Inhibitors are a class of antiretroviral medications used in the treatment of HIV infection. They work by blocking the activity of the HIV protease enzyme, which is necessary for the virus to replicate and infect new cells. By inhibiting this enzyme, the medication prevents the virus from maturing and assembling into new infectious particles.

HIV protease inhibitors are often used in combination with other antiretroviral drugs as part of a highly active antiretroviral therapy (HAART) regimen. This approach has been shown to effectively suppress viral replication, reduce the amount of virus in the bloodstream (viral load), and improve the health and longevity of people living with HIV.

Examples of HIV protease inhibitors include saquinavir, ritonavir, indinavir, nelfinavir, amprenavir, fosamprenavir, atazanavir, darunavir, and tipranavir. These medications are usually taken orally in the form of tablets or capsules, and may be prescribed alone or in combination with other antiretroviral drugs.

It is important to note that HIV protease inhibitors can have significant side effects, including gastrointestinal symptoms such as nausea, diarrhea, and abdominal pain, as well as metabolic changes such as increased cholesterol and triglyceride levels. Therefore, regular monitoring of liver function, lipid levels, and other health parameters is necessary to ensure safe and effective use of these medications.

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