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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The discovery of a fusin protein by researchers at the National Institute of Allergy and Infectious Diseases (NIAID) is considered to be a major advance in the understanding of how HIV disease develops. The discovery does not seem to have immediate implications for treatment. Fusin works together with the CD4 protein to allow HIV to fuse with and enter CD4 cells (T-helper cells). The research was initiated with laboratory mice. Mouse cells were changed genetically so that they would express a human CD4. Fusin exists naturally in human cells and is thought to have a normal function, although this function is yet unknown.
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PMID:NIH scientists find cofactor for HIV entry. National Institutes of Health. 1136 88

Recent data from the National Institute of Allergy and Infectious Diseases (NIAID) indicate that a cell molecule called fusin is required for fusion and entry of certain strains of HIV into cells. Although researchers have known that the virus attaches to CD4, they were also aware that another factor was needed to allow the virus to infect those cells. According to NIAID director, Anthony Fauci, MD, the findings further the understanding of the pathogenesis of HIV disease. The new findings also suggest that small animals, such as mice and rabbits that express both CD4 and fusin, could be used as models for developing anti-HIV drugs and vaccines.
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PMID:Elusive HIV co-factor identified. 1136 54

Researchers have discovered the co-factor, called fusin, that allows HIV to fuse with and insert its genetic material into a cell. The fusin gene is a member of the gene family that produces G protein-coupled cell receptors, often exploited by other viruses when entering cells. Research found fusin to be a valid antiviral target, but no one knows its natural function. A shortcoming of anti-fusin drugs is that anti-fusin antibodies had no effect on the infection of macrophages. There is circumstantial evidence that fusin is similar to the IL-8 chemokine receptor, which may allow HIV to fuse to macrophages. The discovery of fusin makes development of effective animal models more likely.
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PMID:Viral entry discovery suggests new treatments. 1136 81

The recent discovery of fusin, a receptor, expanded the knowledge of how HIV gains access to new cells. CD4 is the other receptor that HIV needs when infecting cells. Characteristics of HIV's binding action are described. Researchers are studying whether chemokines may be the key to protecting cells from HIV.
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PMID:Be kind to your chemokines. 1136 42

Scientists at the National Institute of Allergy and Infectious Diseases (NIAID) report that they have identified fusion cofactors that, for certain strains of HIV-1, make both human and nonhuman CD4+ cells susceptible to HIV fusion and infection. Researchers demonstrated that these HIV-1 strains require, in addition to CD4, a cell surface molecule called CC CKR5 in order to fuse with the membranes of immune system cells. The NIAID researchers found that macrophage-tropic isolates (the strains found in patients during the symptom-free stage of HIV disease) failed to fuse with cells expressing only CD4, but fused with cells that have both CD4 and CC CKR5. Researchers also learned that CC CKR5 is a receptor for certain molecules (chemokines) that are known to suppress HIV infection in cells. The data suggest that one way these chemokines suppress HIV infectivity is by blocking the fusion process used by the virus to enter cells. NIAID also learned earlier this year of another fusion cofactor, termed fusin, which is used by other strains of HIV for entry into immune cells. The findings help provide insights into the pathogenesis of HIV disease and suggest new approaches to developing animal models of HIV infection.
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PMID:NIAID researchers identify cofactors for entry of HIV into cells. National Institute of Allergy and Infectious Diseases. 1136 6

A recent discovery about how HIV infects cells and causes disease has revealed that some racial or ethnic groups, but not others, may be very resistant or even immune to HIV infection through sexual transmission. This discovery opens new doors for scientific progress in understanding HIV pathogenesis that may lead to the creation of a new class of anti-HIV drugs. Two co-receptors, fusin and chemokine receptor 5 (CKR-5), have been found to help HIV enter cells. Those with only one active CKR-5 gene are still capable of becoming HIV infected but in smaller percentages. The occurrence of this genetic defect varies greatly among different human populations. New directions on CKR-5 research are discussed, such as antagonizing the CKR-5 receptor as a treatment option, testing more people for the defective CKR-5 gene, whether CKR-5 is involved in the rare cases of persons who are HIV-negative, and whether people with one defective gene in the CKR-5 receptor molecule progress more slowly in the disease.
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PMID:CKR-5--understanding the news. 1136 20

Back-to-back discoveries of chemokines and the CKR5 receptor site shed new light on how HIV infects cells and why there is so much difference in individual response. The roles of CKR5 and fusin in HIV disease development are discussed. How defects in the CKR5 receptor protein may give these people some immunity to HIV infection is explained. The clinical implications involved in studying this process are highlighted.
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PMID:Basic science discovery: opening the door on HIV. 1136 2

New research shows how the host's response to HIV infection may affect the progression of the disease in an individual. When exposed to HIV, the body responds by producing cytokines, which appear to inhibit HIV replication. Two cytokines, IL-2 and IL-6, have been studied in vitro, and two newly discovered receptors, CCKR5 and fusin, also appear to play a significant role in disease progression. Further testing in humans is needed to fully understand the interplay of these substances.
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PMID:How HIV does its dirty work. 1136 77

Between 1996 and 1999 thirteen cases of HIV infection were detected in Doncaster, a small town in the north of England (population approximately 250,000). A complex network of shared sexual histories involving local nightclubs linked these cases, with the only known risk factor being heterosexual intercourse. A series of frozen blood samples was collected in 1998-1999 and amplified by PCR to generate full-length gp120 clones. Sequencing demonstrated that all the transmission events in this heterosexual group involved the B subtype of HIV-1. When relationships between the samples were assessed it became clear that these 13 cases represented at least three separate strains of HIV-1, indicating that HIV is well established in this community. Eleven of the 13 cases were related, forming two distinct groups. Further investigation revealed that one group contained five patients whose general health was good and who were not receiving HAART. In contrast, the second group of six patients, including the putative index case, were symptomatic, receiving HAART, and may have been infected with a CXCR-4-utilizing virus. Several of the cases that were linked by genetic criteria were not linked by contact tracing, implying that further undiagnosed cases may exist in this community. To our knowledge, this is the largest outbreak of HIV studied within the heterosexual community in the United Kingdom to date, suggesting that this route of infection is becoming more common within the United Kingdom.
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PMID:Phylogenetic analysis of multiple heterosexual transmission events involving subtype b of HIV type 1. 1142 9

This article reviews the cell and molecular biology of human immunodeficiency virus (HIV), emphasizing the features that lead to opportunistic infection by organisms such as mycobacteria. Mycobacteria, especially M. avium complex and M. tuberculosis infections, are closely associated with HIV disease. HIV is a very small retrovirus and its high mutation rate leads to extremely variable viral populations, both within and between individuals. It is coated with glycoprotein 120 (gp120), which it uses to bind to and infect a range of CD4+ leukocytes, depending on the co-receptor specificity. T cell-tropic HIV strains tend to use the CXCR-4 chemokine receptor, while macrophage-tropic strains tend to use the CCR-5 chemokine receptor. Immunosuppression is induced in a number of ways. As well as frank depletion of virus-infected T cells, antigen-specific T cell clones can be selectively deleted by mechanisms such as defective antigen presentation by HIV-infected macrophages (activation-induced cell death). Changes in cytokine production in HIV infection are also proposed. All this leads to falling T cell counts, B cell dysregulation and macrophage dysfunction. Opportunistic infections exploit this immunosuppressed environment. Certain infections are prevalent, reflecting factors such as environmental exposure to pathogens, poor mucosal defences and subcellular interactions between HIV and, e.g. viral or mycobacterial infections. Opportunistic infection exacerbates immune destruction by HIV, producing a vicious cycle that is ultimately fatal.
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PMID:The biology of HIV infection. 1149 53


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