A frequent complication of drug therapy for microbial infection. It may result from opportunistic colonization following immunosuppression by the primary pathogen and can be influenced by the time interval between infections, microbial physiology, or host resistance. Experimental challenge and in vitro models are sometimes used in virulence and infectivity studies.
A phenomenon in which infection by a first virus results in resistance of cells or tissues to infection by a second, unrelated virus.
The phenomenon by which a temperate phage incorporates itself into the DNA of a bacterial host, establishing a kind of symbiotic relation between PROPHAGE and bacterium which results in the perpetuation of the prophage in all the descendants of the bacterium. Upon induction (VIRUS ACTIVATION) by various agents, such as ultraviolet radiation, the phage is released, which then becomes virulent and lyses the bacterium.
The process of intracellular viral multiplication, consisting of the synthesis of PROTEINS; NUCLEIC ACIDS; and sometimes LIPIDS, and their assembly into a new infectious particle.
INFLAMMATION of the LIVER in humans caused by HEPATITIS DELTA VIRUS, a defective RNA virus that can only infect HEPATITIS B patients. For its viral coating, hepatitis delta virus requires the HEPATITIS B SURFACE ANTIGENS produced by these patients. Hepatitis D can occur either concomitantly with (coinfection) or subsequent to (superinfection) hepatitis B infection. Similar to hepatitis B, it is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.
Deoxyribonucleic acid that makes up the genetic material of viruses.
Proteins found in any species of virus.
Established cell cultures that have the potential to propagate indefinitely.
The functional hereditary units of VIRUSES.
Viruses which enable defective viruses to replicate or to form a protein coat by complementing the missing gene function of the defective (satellite) virus. Helper and satellite may be of the same or different genus.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
Visible morphologic changes in cells infected with viruses. It includes shutdown of cellular RNA and protein synthesis, cell fusion, release of lysosomal enzymes, changes in cell membrane permeability, diffuse changes in intracellular structures, presence of viral inclusion bodies, and chromosomal aberrations. It excludes malignant transformation, which is CELL TRANSFORMATION, VIRAL. Viral cytopathogenic effects provide a valuable method for identifying and classifying the infecting viruses.
A species of gram-negative bacteria and causative agent of severe bovine ANAPLASMOSIS. It is the most pathogenic of the ANAPLASMA species.
Viruses which lack a complete genome so that they cannot completely replicate or cannot form a protein coat. Some are host-dependent defectives, meaning they can replicate only in cell systems which provide the particular genetic function which they lack. Others, called SATELLITE VIRUSES, are able to replicate only when their genetic defect is complemented by a helper virus.
The mechanism by which latent viruses, such as genetically transmitted tumor viruses (PROVIRUSES) or PROPHAGES of lysogenic bacteria, are induced to replicate and then released as infectious viruses. It may be effected by various endogenous and exogenous stimuli, including B-cell LIPOPOLYSACCHARIDES, glucocorticoid hormones, halogenated pyrimidines, IONIZING RADIATION, ultraviolet light, and superinfecting viruses.
Ribonucleic acid that makes up the genetic material of viruses.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
Viruses whose hosts are bacterial cells.
Viruses whose host is Escherichia coli.
An analog of DEOXYURIDINE that inhibits viral DNA synthesis. The drug is used as an antiviral agent.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
DNA sequences that form the coding region for proteins associated with the viral core in retroviruses. gag is short for group-specific antigen.
Simultaneous infection of a host organism by two or more pathogens. In virology, coinfection commonly refers to simultaneous infection of a single cell by two or more different viruses.

Bacterial pneumonia as a suprainfection in young adults with measles. (1/244)

The aim of this study was to report the clinical and laboratory characteristics of bacterial pneumonia related to measles infection, and also to assess any correlation between severity and time of onset. Four hundred and twenty-four previously healthy young males (age 22+/-2.1 yrs) were hospitalized with typical symptoms and signs of measles. One hundred and twelve (26%) developed bacterial pneumonia on admission (n=41), during their hospital stay (n=20) or days after their discharge (n=51): groups A, B and C, respectively. Single lobar consolidation was the most common finding, accounting for 89% of cases. Pleural effusion was uncommon and associated in half of the cases with empyema. A microbiological diagnosis was made in 81 cases. Streptococcus pneumoniae (65 cases) and Klebsiella pneumoniae (9 cases) were the most commonly identified organisms. Patients from group C had significantly higher values of white blood cell count and erythrocyte sedimentation rate, and lower values of arterial oxygen tension (14+/-0.8 x 10(9) x L(-1), 88+/-4 mm and 6.3+/-0.4 kPa (47+/-3 mmHg), respectively) than the other two groups. There were no deaths during the hospitalization period. The mean duration of hospital stay was 13+/-2.4 days and was longer in the presence of K. pneumoniae infection (19+/-1.6 days). Six patients from group C were admitted to the intensive care unit. In conclusion, these data suggest that bacterial pneumonia associated with measles is not unusual in hospitalized adults, and it seems to be more severe when it occurs days after the onset of rash.  (+info)

Influenza A virus accelerates neutrophil apoptosis and markedly potentiates apoptotic effects of bacteria. (2/244)

Neutrophils are recruited into the airway in the early phase of uncomplicated influenza A virus (IAV) infection and during the bacterial superinfections that are a significant cause of morbidity and mortality in IAV-infected subjects. In this report, we show that IAV accelerates neutrophil apoptosis. Unopsonized Escherichia coli had similar effects, although apoptotic effects of opsonized E coli were greater. When neutrophils were treated with both IAV and unopsonized E coli, a marked enhancement of the rate and extent of neutrophil apoptosis occurred as compared with that caused by either pathogen alone. Treatment of neutrophils with IAV markedly increased phagocytosis of E coli. Simultaneous treatment of neutrophils with IAV and E coli also elicited greater hydrogen peroxide production than did either pathogen alone. IAV increased neutrophil expression of Fas antigen and Fas ligand, and it also increased release of Fas ligand into the cell supernatant. These findings may have relevance to the understanding of inflammatory responses to IAV in vivo and of bacterial superinfection of IAV-infected subjects.  (+info)

Protection against development of otitis media induced by nontypeable Haemophilus influenzae by both active and passive immunization in a chinchilla model of virus-bacterium superinfection. (3/244)

Three separate studies, two involving active-immunization regimens and one involving a passive-transfer protocol, were conducted to initially screen and ultimately more fully assess several nontypeable Haemophilus influenzae outer membrane proteins or their derivatives for their relative protective efficacy in chinchilla models of otitis media. Initial screening of these antigens (P5-fimbrin, lipoprotein D, and P6), delivered singly or in combination with either Freund's adjuvant or alum, indicated that augmented bacterial clearance from the nasopharynx, the middle ears, or both anatomical sites could be induced by parenteral immunization with P5-fimbrin combined with lipoprotein D, lipoprotein D alone, or the synthetic chimeric peptide LB1 (derived from P5-fimbrin), respectively. Data from a second study, wherein chinchillas were immunized with LB1 or lipoprotein D, each delivered with alum, again indicated that clearance of nontypeable H. influenzae could be augmented by immunization with either of these immunogens; however, when this adjuvant was used, both antibody titers in serum and efficacy were reduced. A third study was performed to investigate passive delivery of antisera directed against either LB1, lipoprotein D, nonacylated lipoprotein D, or a unique recombinant peptide designated LPD-LB1(f)2,1,3. The last three antiserum pools were generated by using the combined adjuvant of alum plus monophosphoryl lipid A. Passive transfer of sera specific for LB1 or LPD-LB1(f)2,1,3 to adenovirus-compromised chinchillas, prior to intranasal challenge with nontypeable H. influenzae, significantly reduced the severity of signs and incidence of otitis media which developed (P +info)

Interleukin 5 (IL-5) is not required for expression of a Th2 response or host resistance mechanisms during murine schistosomiasis mansoni but does play a role in development of IL-4-producing non-T, non-B cells. (4/244)

During schistosomiasis, interleukin-5 (IL-5)-dependent eosinophil responses have been implicated in immunopathology, resistance to superinfection, synergistic interactions with chemotherapeutic agents, and the inductive phase of the egg-induced Th2 response. We examined these issues in IL-5-deficient (IL-5(-/-)) mice. IL-5(-/-) and wild-type (WT) mice were indistinguishable in terms of susceptibility to primary infections and the ability to resist secondary infections. Moreover, hepatic pathology was similar in both strains apart from a relative lack of eosinophils and, during chronic infection, a significantly larger mast cell component in the granulomas of IL-5(-/-) mice. Splenocyte cytokine production in response to soluble egg antigen (SEA) or anti-CD3 revealed no significant differences except for heightened tumor necrosis factor alpha production by cells from chronically infected IL-5(-/-) mice compared to WT animals. In contrast, ionomycin-stimulated non-B, non-T (NBNT) cells from IL-5(-/-) mice produced significantly smaller IL-4 amounts than did NBNT cells from WT animals. This difference was not apparent following plate-bound anti-immunoglobulin E or SEA stimulation. The absence of IL-5 failed to affect the induction of Th2 responses in naive mice. Peritoneal exudate cells recovered from egg-injected IL-5(-/-) or WT mice produced equivalent levels of IL-4 following restimulation with SEA or anti-CD3.  (+info)

Selective irreversible inactivation of replicating mengovirus by nucleoside analogues: a new form of viral interference. (5/244)

We describe the selective irreversible inhibition of mengovirus growth in cultured cells by a combination of two pyrrolopyrimidine nucleoside analogues, 5-bromotubercidin (BrTu) and tubercidin (Tu). At a concentration of 5 microgram/ml, BrTu reversibly blocked the synthesis of cellular mRNA and rRNA but did not inhibit either mengovirus RNA synthesis or multiplication. BrTu is a potent inhibitor of adenosine kinase, and low concentrations of BrTu (e.g., 0.5 microgram/ml), which did not by themselves inhibit cell growth, blocked phosphorylation of Tu and thus protected uninfected cells against irreversible cytotoxicity resulting from Tu incorporation into nucleic acids. In contrast, in mengovirus-infected cells, BrTu did not completely inhibit Tu incorporation into mengovirus RNA, allowing the formation of Tu-containing functionally defective polynucleotides that aborted the virus development cycle. This increased incorporation of Tu coupled to mengovirus infection could be attributed either to a reduction in the inhibitory action of BrTu and/or its nucleotide derivatives at the level of nucleoside and nucleotide kinases and/or, perhaps, to an effect upon the nucleoside transport system. The virus life cycle in nucleoside-treated cells progressed to the point of synthesis of negative strands and probably to the production of a few defective new positive strands. Irreversible virus growth arrest was achieved if the nucleoside mixture of BrTu (0.5 to 10 microgram/ml) and Tu (1 to 20 microgram/ml) was added no later than 30 min after virus infection and maintained for periods of 2 to 8 h. The cultures thus "cured" of mengovirus infection could be maintained and transferred for several weeks, during which they neither produced detectable virus nor showed a visible cytopathic effect; however, the infected and cured cells themselves, while metabolically viable, were permanently impaired in RNA synthesis and unable to divide. Although completely resistant to superinfecting picornaviruses, they retained the ability to support the growth of several other viruses (vaccinia virus, reovirus, and vesicular stomatitis virus), showing that cured cells had, in general, retained the metabolic and structural machinery needed for virus production. The resistance of cured cells to superinfection with picornaviruses seemed attributable neither to interferon action nor to destruction or blockade of virus receptors but more likely to the consumption of some host factor(s) involved in the expression of early viral functions during the original infection.  (+info)

An open, randomized, multicentre study comparing the use of low-dose ceftazidime or cefotaxime, both in combination with netilmicin, in febrile neutropenic patients. German Multicentre Study Group. (6/244)

To reduce drug acquisition costs, the clinical and bacteriological efficacy of low-dose ceftazidime i.v. (1 g tid) was compared with cefotaxime i.v. (2 g tid). Both regimens were combined with netilmicin i.v. (2 mg/kg bodyweight tid), in an open, randomized, multicentre trial in febrile neutropenic patients. The addition of antibiotics for gram-positive coverage was part of the protocol; alteration in the antibiotics for gram-negative cover or premature discontinuation of the study antibiotics were judged as failure. One hundred and eighty six patients were randomized by nine German centres, the patients matched for age, underlying diseases and duration of neutropenia (median duration 14 days) in both treatment arms. Infections were documented microbiologically in 29% of the patients, clinically in 16% and suspected (fever of unknown origin) in 102/186 patients (55%). The 82 pathogens isolated were predominantly gram-positive bacteria. In an intent-to-treat analysis, the overall response rate without modification at the final evaluation was 58% in the ceftazidime group and 34% in the cefotaxime group (P < 0.01). The success rates with modification were 84% and 64%, respectively. The failure rate in a highly immunosuppressed subgroup of the patients (bone marrow transplant recipients) was higher for cefotaxime (53%) than for the ceftazidime arm (14%) (P < 0.001). Response rates were significantly higher in the ceftazidime group for patients with microbiologically documented and possible infections. No major bacterial superinfections occurred in the low-dose treatment arm. The tolerability was good for both regimens. Low-dose ceftazidime combined with netilmicin proved to be superior to recommended doses of cefotaxime/netilmicin in febrile neutropenic patients.  (+info)

Expression of mouse mammary tumor virus envelope protein does not prevent superinfection in vivo or in vitro. (7/244)

Inbred mice expressing endogenous mouse mammary tumor virus envelope proteins can be infected with exogenous virus, and the mammary tumors that develop in these mice usually have many proviruses integrated in their genomes, indicating that this virus is not subject to receptor interference. We show here that transgenic mice expressing an exogenous mouse mammary tumor virus (C3H) envelope protein can still be infected with this virus. Moreover, cultured mammary gland cells expressing the mouse mammary tumor virus (C3H) envelope protein can be superinfected with pseudotyped viruses bearing that same protein. Thus cellular expression of the mouse mammary tumor virus envelope protein does not block superinfection in vivo or in vitro.  (+info)

Inhibitory and bactericidal effects of hydrogen peroxide production by Streptococcus pneumoniae on other inhabitants of the upper respiratory tract. (8/244)

An inverse correlation between colonization of the human nasopharynx by Streptococcus pneumoniae and Haemophilus influenzae, both common upper respiratory pathogens, has been reported. Studies were undertaken to determine if either of these organisms produces substances which inhibit growth of the other. Culture supernatants from S. pneumoniae inhibited growth of H. influenzae, whereas culture supernatants from H. influenzae had no effect on the growth of S. pneumoniae. Moreover, coculture of S. pneumoniae and H. influenzae led to a rapid decrease in viable counts of H. influenzae. The addition of purified catalase prevented killing of H. influenzae in coculture experiments, suggesting that hydrogen peroxide may be responsible for this bactericidal activity. H. influenzae was killed by concentrations of hydrogen peroxide similar to that produced by S. pneumoniae. Hydrogen peroxide is produced by the pneumococcus through the action of pyruvate oxidase (SpxB) under conditions of aerobic growth. Both an spxB mutant and a naturally occurring variant of S. pneumoniae, which is downregulated in SpxB expression, were unable to kill H. influenzae. A catalase-reversible inhibitory effect of S. pneumoniae on the growth of the respiratory tract pathogens Moraxella catarrhalis and Neisseria meningitidis was also observed. Elevated hydrogen peroxide production, therefore, may be a means by which S. pneumoniae is able to inhibit a variety of competing organisms in the aerobic environment of the upper respiratory tract.  (+info)

Superinfection is a medical term that refers to a secondary infection which occurs during or following the treatment of an initial infection. This second infection is often caused by a different microorganism that is resistant to the medication used to treat the first infection. Superinfections can occur in various parts of the body, such as the skin, respiratory system, gastrointestinal tract, or urinary tract, and are more common in individuals with weakened immune systems, chronic illnesses, or those who have been on antibiotics for an extended period.

Superinfections can lead to more severe complications, prolonged hospital stays, increased healthcare costs, and higher mortality rates if not promptly diagnosed and treated appropriately. Healthcare providers must be vigilant in monitoring patients' responses to treatment and recognizing signs of superinfection, such as worsening symptoms or the development of new ones, to ensure timely intervention and optimal patient outcomes.

Viral interference is a phenomenon where the replication of one virus is inhibited or blocked by the presence of another virus. This can occur when two different viruses infect the same cell and compete for the cell's resources, such as nucleotides, energy, and replication machinery. As a result, the replication of one virus may be suppressed, allowing the other virus to predominate.

This phenomenon has been observed in both in vitro (laboratory) studies and in vivo (in the body) studies. It has been suggested that viral interference may play a role in the outcome of viral coinfections, where an individual is infected with more than one virus at the same time. Viral interference can also be exploited as a potential strategy for antiviral therapy, where one virus is used to inhibit the replication of another virus.

It's important to note that not all viruses interfere with each other, and the outcome of viral coinfections can depend on various factors such as the specific viruses involved, the timing and sequence of infection, and the host's immune response.

Lysogeny is a process in the life cycle of certain viruses, known as bacteriophages or phages, which can infect bacteria. In lysogeny, the viral DNA integrates into the chromosome of the host bacterium and replicates along with it, remaining dormant and not producing any new virus particles. This state is called lysogeny or the lysogenic cycle.

The integrated viral DNA is known as a prophage. The bacterial cell that contains a prophage is called a lysogen. The lysogen can continue to grow and divide normally, passing the prophage onto its daughter cells during reproduction. This dormant state can last for many generations of the host bacterium.

However, under certain conditions such as DNA damage or exposure to UV radiation, the prophage can be induced to excise itself from the bacterial chromosome and enter the lytic cycle. In the lytic cycle, the viral DNA replicates rapidly, producing many new virus particles, which eventually leads to the lysis (breaking open) of the host cell and the release of the newly formed virions.

Lysogeny is an important mechanism for the spread and survival of bacteriophages in bacterial populations. It also plays a role in horizontal gene transfer between bacteria, as genes carried by prophages can be transferred to other bacteria during transduction.

Virus replication is the process by which a virus produces copies or reproduces itself inside a host cell. This involves several steps:

1. Attachment: The virus attaches to a specific receptor on the surface of the host cell.
2. Penetration: The viral genetic material enters the host cell, either by invagination of the cell membrane or endocytosis.
3. Uncoating: The viral genetic material is released from its protective coat (capsid) inside the host cell.
4. Replication: The viral genetic material uses the host cell's machinery to produce new viral components, such as proteins and nucleic acids.
5. Assembly: The newly synthesized viral components are assembled into new virus particles.
6. Release: The newly formed viruses are released from the host cell, often through lysis (breaking) of the cell membrane or by budding off the cell membrane.

The specific mechanisms and details of virus replication can vary depending on the type of virus. Some viruses, such as DNA viruses, use the host cell's DNA polymerase to replicate their genetic material, while others, such as RNA viruses, use their own RNA-dependent RNA polymerase or reverse transcriptase enzymes. Understanding the process of virus replication is important for developing antiviral therapies and vaccines.

Hepatitis D, also known as Delta hepatitis, is a viral infection of the liver that can only occur in people who have a current infection with the hepatitis B virus (HBV). It's caused by the hepatitis delta virus (HDV), which is a small, enveloped, single-stranded RNA virus.

HDV requires the presence of HBV for its replication and survival, so it can't infect someone who doesn't already have HBV. When both viruses are present, they can interact in ways that lead to more severe liver disease than either virus would cause alone.

Hepatitis D can be an acute or chronic infection, and it can range from mild to severe, with symptoms similar to those of other types of viral hepatitis, such as jaundice, fatigue, loss of appetite, nausea, vomiting, abdominal pain, and joint pain. In some cases, hepatitis D can lead to serious complications, including liver failure and death.

Hepatitis D is primarily spread through contact with infected blood or other bodily fluids, such as during sexual contact, sharing needles, or mother-to-child transmission during childbirth. It's preventable through vaccination against hepatitis B, which provides immunity to both viruses. There is no specific treatment for hepatitis D, but antiviral therapy for hepatitis B can help manage the infection and prevent complications.

Viral DNA refers to the genetic material present in viruses that consist of DNA as their core component. Deoxyribonucleic acid (DNA) is one of the two types of nucleic acids that are responsible for storing and transmitting genetic information in living organisms. Viruses are infectious agents much smaller than bacteria that can only replicate inside the cells of other organisms, called hosts.

Viral DNA can be double-stranded (dsDNA) or single-stranded (ssDNA), depending on the type of virus. Double-stranded DNA viruses have a genome made up of two complementary strands of DNA, while single-stranded DNA viruses contain only one strand of DNA.

Examples of dsDNA viruses include Adenoviruses, Herpesviruses, and Poxviruses, while ssDNA viruses include Parvoviruses and Circoviruses. Viral DNA plays a crucial role in the replication cycle of the virus, encoding for various proteins necessary for its multiplication and survival within the host cell.

Viral proteins are the proteins that are encoded by the viral genome and are essential for the viral life cycle. These proteins can be structural or non-structural and play various roles in the virus's replication, infection, and assembly process. Structural proteins make up the physical structure of the virus, including the capsid (the protein shell that surrounds the viral genome) and any envelope proteins (that may be present on enveloped viruses). Non-structural proteins are involved in the replication of the viral genome and modulation of the host cell environment to favor viral replication. Overall, a thorough understanding of viral proteins is crucial for developing antiviral therapies and vaccines.

A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.

Viral genes refer to the genetic material present in viruses that contains the information necessary for their replication and the production of viral proteins. In DNA viruses, the genetic material is composed of double-stranded or single-stranded DNA, while in RNA viruses, it is composed of single-stranded or double-stranded RNA.

Viral genes can be classified into three categories: early, late, and structural. Early genes encode proteins involved in the replication of the viral genome, modulation of host cell processes, and regulation of viral gene expression. Late genes encode structural proteins that make up the viral capsid or envelope. Some viruses also have structural genes that are expressed throughout their replication cycle.

Understanding the genetic makeup of viruses is crucial for developing antiviral therapies and vaccines. By targeting specific viral genes, researchers can develop drugs that inhibit viral replication and reduce the severity of viral infections. Additionally, knowledge of viral gene sequences can inform the development of vaccines that stimulate an immune response to specific viral proteins.

Helper viruses, also known as "auxiliary" or "satellite" viruses, are defective viruses that depend on the assistance of a second virus, called a helper virus, to complete their replication cycle. They lack certain genes that are essential for replication, and therefore require the helper virus to provide these functions.

Helper viruses are often found in cases of dual infection, where both the helper virus and the dependent virus infect the same cell. The helper virus provides the necessary enzymes and proteins for the helper virus to replicate, package its genome into new virions, and bud off from the host cell.

One example of a helper virus is the hepatitis B virus (HBV), which can serve as a helper virus for hepatitis D virus (HDV) infection. HDV is a defective RNA virus that requires the HBV surface antigen to form an envelope around its nucleocapsid and be transmitted to other cells. In the absence of HBV, HDV cannot replicate or cause disease.

Understanding the role of helper viruses in viral infections is important for developing effective treatments and vaccines against viral diseases.

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.

A Cytopathic Effect (CPE) is a visible change in the cell or group of cells due to infection by a pathogen, such as a virus. When the cytopathic effect is caused specifically by a viral infection, it is referred to as a "Viral Cytopathic Effect" (VCPE).

The VCPE can include various changes in the cell's morphology, size, and structure, such as rounding, shrinkage, multinucleation, inclusion bodies, and formation of syncytia (multinucleated giant cells). These changes are often used to identify and characterize viruses in laboratory settings.

The VCPE is typically observed under a microscope after the virus has infected cell cultures, and it can help researchers determine the type of virus, the degree of infection, and the effectiveness of antiviral treatments. The severity and timing of the VCPE can vary depending on the specific virus and the type of cells that are infected.

'Anaplasma marginale' is a gram-negative bacterium that infects red blood cells in various species of animals, including cattle. It is the causative agent of Anaplasmosis, which is a tick-borne disease that can lead to severe anemia, abortion, and even death in infected animals. The bacteria are transmitted through the bite of infected ticks or through contaminated blood transfusions, needles, or surgical instruments.

The bacterium has a unique life cycle, where it infects and replicates within the red blood cells, causing them to rupture and release more bacteria into the bloodstream. This results in the characteristic symptoms of Anaplasmosis, such as fever, weakness, icterus (yellowing of the mucous membranes), and anemia.

Diagnosis of Anaplasmosis can be confirmed through various laboratory tests, including blood smears, PCR assays, and serological tests. Treatment typically involves the use of antibiotics such as tetracyclines, which can help to reduce the severity of symptoms and clear the infection. Preventive measures include the control of tick populations, the use of protective clothing and insect repellents, and the implementation of strict biosecurity protocols in veterinary practices and farms.

Defective viruses are viruses that have lost the ability to complete a full replication cycle and produce progeny virions independently. These viruses require the assistance of a helper virus, which provides the necessary functions for replication. Defective viruses can arise due to mutations, deletions, or other genetic changes that result in the loss of essential genes. They are often non-infectious and cannot cause disease on their own, but they may interfere with the replication of the helper virus and modulate the course of infection. Defective viruses can be found in various types of viruses, including retroviruses, bacteriophages, and DNA viruses.

Viral activation, also known as viral reactivation or virus reactivation, refers to the process in which a latent or dormant virus becomes active and starts to replicate within a host cell. This can occur when the immune system is weakened or compromised, allowing the virus to evade the body's natural defenses and cause disease.

In some cases, viral activation can be triggered by certain environmental factors, such as stress, exposure to UV light, or infection with another virus. Once activated, the virus can cause symptoms similar to those seen during the initial infection, or it may lead to new symptoms depending on the specific virus and the host's immune response.

Examples of viruses that can remain dormant in the body and be reactivated include herpes simplex virus (HSV), varicella-zoster virus (VZV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV). It is important to note that not all viruses can be reactivated, and some may remain dormant in the body indefinitely without causing any harm.

A viral RNA (ribonucleic acid) is the genetic material found in certain types of viruses, as opposed to viruses that contain DNA (deoxyribonucleic acid). These viruses are known as RNA viruses. The RNA can be single-stranded or double-stranded and can exist as several different forms, such as positive-sense, negative-sense, or ambisense RNA. Upon infecting a host cell, the viral RNA uses the host's cellular machinery to translate the genetic information into proteins, leading to the production of new virus particles and the continuation of the viral life cycle. Examples of human diseases caused by RNA viruses include influenza, COVID-19 (SARS-CoV-2), hepatitis C, and polio.

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.

Bacteriophages, often simply called phages, are viruses that infect and replicate within bacteria. They consist of a protein coat, called the capsid, that encases the genetic material, which can be either DNA or RNA. Bacteriophages are highly specific, meaning they only infect certain types of bacteria, and they reproduce by hijacking the bacterial cell's machinery to produce more viruses.

Once a phage infects a bacterium, it can either replicate its genetic material and create new phages (lytic cycle), or integrate its genetic material into the bacterial chromosome and replicate along with the bacterium (lysogenic cycle). In the lytic cycle, the newly formed phages are released by lysing, or breaking open, the bacterial cell.

Bacteriophages play a crucial role in shaping microbial communities and have been studied as potential alternatives to antibiotics for treating bacterial infections.

Coliphages are viruses that infect and replicate within certain species of bacteria that belong to the coliform group, particularly Escherichia coli (E. coli). These viruses are commonly found in water and soil environments and are frequently used as indicators of fecal contamination in water quality testing. Coliphages are not harmful to humans or animals, but their presence in water can suggest the potential presence of pathogenic bacteria or other microorganisms that may pose a health risk. There are two main types of coliphages: F-specific RNA coliphages and somatic (or non-F specific) DNA coliphages.

Idoxuridine is an antiviral medication used primarily for the treatment of herpes simplex virus (HSV) infections of the eye, such as keratitis or dendritic ulcers. It works by interfering with the DNA replication of the virus, thereby inhibiting its ability to multiply and spread.

Idoxuridine is available as an ophthalmic solution (eye drops) and is typically applied directly to the affected eye every 1-2 hours while awake, for up to 2 weeks. Common side effects include local irritation, stinging, or burning upon application. Prolonged use of idoxuridine may lead to bacterial resistance or corneal toxicity, so it is important to follow your healthcare provider's instructions carefully when using this medication.

It is essential to note that idoxuridine is not commonly used today due to the development of more effective and less toxic antiviral agents for HSV infections.

Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.

"Gag" is a term that refers to a group of genes found in retroviruses, a type of virus that includes HIV (human immunodeficiency virus). These genes encode proteins that play a crucial role in the replication and packaging of the viral genome into new virus particles.

The "gag" gene encodes a polyprotein, which is cleaved by viral proteases into several individual proteins during the maturation of the virus. The resulting proteins include matrix (MA), capsid (CA), and nucleocapsid (NC) proteins, as well as smaller peptides that help to facilitate the assembly and release of new virus particles.

The gag gene is an essential component of retroviruses, and its function has been extensively studied in order to better understand the replication cycle of these viruses and to develop potential therapies for retroviral infections.

Coinfection is a term used in medicine to describe a situation where a person is infected with more than one pathogen (infectious agent) at the same time. This can occur when a person is infected with two or more viruses, bacteria, parasites, or fungi. Coinfections can complicate the diagnosis and treatment of infectious diseases, as the symptoms of each infection can overlap and interact with each other.

Coinfections are common in certain populations, such as people who are immunocompromised, have chronic illnesses, or live in areas with high levels of infectious agents. For example, a person with HIV/AIDS may be more susceptible to coinfections with tuberculosis, hepatitis, or pneumocystis pneumonia. Similarly, a person who has recently undergone an organ transplant may be at risk for coinfections with cytomegalovirus, Epstein-Barr virus, or other opportunistic pathogens.

Coinfections can also occur in people who are otherwise healthy but are exposed to multiple infectious agents at once, such as through travel to areas with high levels of infectious diseases or through close contact with animals that carry infectious agents. For example, a person who travels to a tropical area may be at risk for coinfections with malaria and dengue fever, while a person who works on a farm may be at risk for coinfections with influenza and Q fever.

Effective treatment of coinfections requires accurate diagnosis and appropriate antimicrobial therapy for each pathogen involved. In some cases, treating one infection may help to resolve the other, but in other cases, both infections may need to be treated simultaneously to achieve a cure. Preventing coinfections is an important part of infectious disease control, and can be achieved through measures such as vaccination, use of personal protective equipment, and avoidance of high-risk behaviors.

Superinfection is the process by which a cell that has previously been infected by one virus gets co-infected with a different ... A superinfection is a second infection superimposed on an earlier one, especially by a different microbial agent of exogenous ... Viral superinfections may also be less susceptible to the hosts immune response. In Zika virus infection, there is some ... In parasitology, superinfection is reinfection of the same genus of parasite, as a person infected by Fasciola hepatica again ...
... revealed possible novel mechanisms for cross protection and the closely related process of superinfection exclusion (SIE). Our ... revealed possible novel mechanisms for cross protection and the closely related process of superinfection exclusion (SIE). Our ... A New Mechanistic Model for Viral Cross Protection and Superinfection Exclusion. Xiao-Feng Zhang1* Shaoyan Zhang2 Qin Guo2 Rong ... 2007). Superinfection exclusion in cells infected with hepatitis C virus. J. Virol. 81, 3693-3703. doi: 10.1128/JVI.01748-06 ...
... World J Gastroenterol 2016; 22(47): 10388-10397 ... Clinical features of acute hepatitis E super-infections on chronic hepatitis B. World J Gastroenterol 2016; 22(47): 10388-10397 ...
Invasive Aspergillosis as an Under-recognized Superinfection in COVID-19. Open Forum Infect. Dis., 7 (7). CARY: OXFORD UNIV ...
Tags: antivirals, bacterial superinfection, drug resistance, fatal cases, h1n1 (2009), oseltamivir, seasonal influenza, severe ... United Kingdom reports 25% ICU beds occupancy due to H1N1 (2009) influenza, bacterial superinfections and 2% of oseltamivir ... United Kingdom reports 25% ICU beds occupancy due to H1N1 (2009) influenza, bacterial superinfections and 2% of oseltamivir ...
Why are superinfections unrelated to the first infection?. Why are superinfections unrelated to the first infection?. Such ... Can a superinfection cause diarrhea and death?. Superinfections range from mild infections that do not need further treatment ... When does superinfection complicate the course of antimicrobial therapy?. Superinfection can complicate the course of ... Superinfections range from mild infections that do not need further treatment to very severe infections that can lead to death ...
Superinfection presents an increased risk of hyperparasitemia and death in less immune individuals but counterintuitively is ... Host-mediated regulation of superinfection in malaria Portugal S., Carret C., Recker M., Armitage AE., Gonçalves LA., Epiphanio ... Superinfection presents an increased risk of hyperparasitemia and death in less immune individuals but counterintuitively is ...
Superinfection occurs when people with chronic, active HBV infection are subsequently infected with HDV. Superinfection ... What is HBV/hepatitis D virus (HDV) superinfection?. ...
Superinfection exclusion (SIE) is a natural phenomenon where one virus prevents subsequent entry of another virus. Studies have ... Evaluation of conditions and mechanisms of alphaherpesvirus superinfection exclusion (PDF) (18.48Mb) ...
84 p., Dissertation Abstracts International, Volume: 32-04, Section: B, page: 2441. ...
Superinfections. Superinfections are defined as infections with one or more additional pathogens during the course of ... Why is it Important to Differentiate UTIs According to whether they are Persistent, Relapses, Reinfections, or Superinfections? ...
Search by Diagnosis: "herpes simplex virus superinfection". Show Diagnoses. Week 546: Case 1. Diagnosis: herpes simplex virus ...
Dr Oz: Super Infections: When the Common Cold Can Kill. Newsletter , Contact , Privacy Policy , Terms of Use ...
We investigated the effect of vaccination on virus-induced host immune responses and on the outcome of superinfection with ... We investigated the effect of vaccination on virus-induced host immune responses and on the outcome of superinfection with ... We investigated the effect of vaccination on virus-induced host immune responses and on the outcome of superinfection with ... We investigated the effect of vaccination on virus-induced host immune responses and on the outcome of superinfection with ...
Recently an unusual example of superinfection of an amoebic abscess ... Superinfection of an Amoebic Abscess by Salmonella enteritidis. Arch Intern Med. 1971;128(2):291-294. doi:10.1001/archinte. ... Recently an unusual example of superinfection of an amoebic abscess by Salmonella enteritidis was admitted to this hospital. ...
Interleukin-22 and Post-Influenza Bacterial Superinfection. Interleukin-22 protects against bacterial superinfections that can ...
Hepatitis E virus superinfection in patients with chronic liver disease. / Hamid, Saeed S.; Atiq, Muslim; Shehzad, Farooq et al ... Hepatitis E virus superinfection in patients with chronic liver disease. Saeed S. Hamid, Muslim Atiq, Farooq Shehzad, Aneela ... Hepatitis E virus superinfection in patients with chronic liver disease. In: Hepatology. 2002 ; Vol. 36, No. 2. pp. 474-478. ... Hepatitis E virus superinfection in patients with chronic liver disease. Hepatology. 2002;36(2):474-478. doi: 10.1053/jhep. ...
HIV superinfection more common in Uganda June 22, 2012 ARTICLES 2008-2015, In The Magazine, NEWS ANALYSIS 0 ... By Independent Reporter Study in Rakai shows HIV infected individual catches new viruses at higher rate HIV superinfection, ...
superinfection. ." This can complicate treatment.. Current medications can reduce the levels of HIV in the body so that the ... HIV superinfection. (2022).. https://www.cdc.gov/hiv/basics/hiv-transmission/hiv-superinfection.html. ...
Characterization of retroviral infectivity and superinfection resistance during retrovirus-mediated transduction of mammalian ... Characterization of retroviral infectivity and superinfection resistance during retrovirus-mediated transduction of mammalian ... Characterization of retroviral infectivity and superinfection resistance during retrovirus-mediated transduction of mammalian ...
Superinfection. 7/16 (31). Pustule(s). 3/16 (19). Suppuration. 4/16 (25). ...
... and an increased risk for pulmonary infarction and related superinfection. [6] Moreover, patients with COVID-19 and VAP have ...
Superinfection is rare -- it happens in less than 4% of people. Youre at the highest risk of superinfection in the first 3 ... University of California San Francisco Center for AIDS Prevention Studies: "What do we know about HIV superinfection?" ...
Bacterial infections may develop de novo or as a superinfection of a viral URI. ... Bacterial primary infection or superinfection may require targeted therapy (see Treatment). ...
Risk of Superinfection Minimal in Organ Transplants Between HIV+ Donors and Recipients Editors pick ...
Bacterial superinfection. * Pneumonia develops in about 5% of patients with bronchitis (incidence of subsequent pneumonia, ...
Targeting Bacterial Super-Infections with Specialized Pro-Resolving Mediators. Hence, a therapeutic strategy that dampens the ... In the classic bacterial super-infection setting, S. pneumoniae can enter and proliferate in the brain, with the ensuing ... Similar to classic bacterial super-infection models, acute viral infection resulted in a marked increase in pneumococcal lung ... the virus permits the further outgrowth of bacteria causing a bacterial super-infection in the lungs. SAA is significantly ...
Although superinfection with wild-type SIVmacJ5 was detected at postmortem in a single anti-CD8 MAb-treated vaccinee, this did ... for host-mediated control of SIV primary viremia but do not indicate a central role in protection against acute superinfection ... four control vaccinees and three out of four anti-CD8 MAb-treated vaccinees were protected against detectable superinfection ... In order to test the hypothesis that CD8+ cytotoxic T lymphocytes mediate protection against acute superinfection, we depleted ...

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