Links to PubMed are also available for Selected References. Get a printable copy (PDF file) of the complete article (27M), or click on a page image below to browse page by page. Full textįull text is available as a scanned copy of the original print version. Ongoing research is necessary to find a solution to this devastating worldwide epidemic. Vaccine development has provided some encouraging results, but the observations indicate the major challenge of preventing infection by HIV. Several therapeutic approaches have been attempted, and others are under investigation. Long-term survival appears to involve infection with a relatively low-virulence strain that remains sensitive to the immune response, particularly to control by CD8+ cell antiviral activity. The host reaction against HIV, through neutralizing antibodies and particularly through strong cellular immune responses, can keep the virus suppressed for many years.
HIV strains are highly heterogeneous, and certain biologic and serologic properties determined by specific genetic sequences can be linked to pathogenic pathways and resistance to the immune response.
With CD4+ lymphocytes, HIV replication can cause syncytium formation and cell death with other cells, such as macrophages, persistent infection can occur, creating reservoirs for the virus in many cells and tissues.
Following virus infection, a variety of intracellular mechanisms determine the relative expression of viral regulatory and accessory genes leading to productive or latent infection. Virus-cell fusion and HIV entry subsequently take place. The steps occurring in infection involve an interaction of HIV not only with the CD4 molecule on cells but also with other cellular receptors recently identified. HIV is transmitted primarily through blood and genital fluids and to newborn infants from infected mothers. The lentivirus human immunodeficiency virus (HIV) causes AIDS by interacting with a large number of different cells in the body and escaping the host immune response against it.
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