Human immunodeficiency virus infection

Human immunodeficiency virus infection


One of the most widely publicized diseases, human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS) is caused by the marked progressive failure of the immune system. Although it’s characterized by gradual destruction of cell-mediated (T-cell) immunity, it also affects humoral immunity and autoimmunity because of the central role of the CD4+ T lymphocyte in immune reactions. The resultant immunodeficiency makes the patient susceptible to opportunistic infections, unusual cancers, and other abnormalities that define AIDS.

This syndrome was first described by the Centers for Disease Control and Prevention (CDC) in 1981. Since then, the CDC has declared a case surveillance definition for AIDS and has modified it several times, most recently in 1993.

A retrovirus—the HIV type 1—is the primary causative agent. Transmission of HIV occurs by contact with infected blood or body fluids and is associated with identifiable high-risk behaviors. It’s therefore disproportionately represented in homosexual and bisexual men, I.V. drug users, neonates of HIV-infected women, recipients of contaminated blood or blood products (dramatically decreased since mid-1985), and heterosexual partners of persons in the former groups. Because of similar routes of transmission, AIDS shares epidemiologic patterns with hepatitis B and sexually transmitted diseases (STDs).

The natural history of AIDS infection begins with infection by the HIV retrovirus, which is detectable only by laboratory tests, and ends with the severely immunocompromised, terminal stage of this disease. Depending on individual variations and the presence of co-factors that influence progression, the time elapsed from acute HIV infection to the appearance of symptoms (mild to severe) to the diagnosis and, eventually, to death varies greatly. Current combination antiretroviral therapy (for example, with zidovudine, ritonavir, and others) and treatment and prophylaxis of common opportunistic
infections can delay the natural progression of HIV disease and prolong survival.


The virus has two major strains: HIV-1, which is closely related to the primate retrovirus called simian immunodeficiency virus, and HIV-2, which is associated with immunodeficiency but less pathogenic that HIV-1, results from infection with HIV, which strikes cells bearing the CD4+ antigen; the latter (normally a receptor for major histocompatibility complex molecules) serves as a receptor for the retrovirus and lets it enter the cell. HIV prefers to infect the CD4+ lymphocyte or macrophage but may also infect other CD4+ antigen-bearing cells of the GI tract, uterine cervical cells, and neuroglial cells. The virus gains access by binding to the CD4+ molecule on the cell surface along with a co-receptor (thought to be the receptor CCR5). After invading a cell, HIV either replicates, which leads to cell death, or becomes latent. HIV infection leads to profound pathology, either directly, through destruction of CD4+ T cells, other immune cells, and neuroglial cells, or indirectly, through the secondary effects of CD4+ T-cell dysfunction and resultant immunosuppression.

The infection process takes three forms:

  • immunodeficiency (opportunistic infections and unusual cancers)

  • autoimmunity (lymphoid interstitial pneumonia, arthritis, hypergammaglobulinemia, and production of autoimmune antibodies)

  • neurologic dysfunction (AIDS dementia complex, HIV encephalopathy, and peripheral neuropathies).

Jun 16, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Human immunodeficiency virus infection

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