Atlas of pathophysiology, 2 Edition

Part II - Disorders

Immunologic Disorders

Acquired immunodeficiency syndrome

Human immunodeficiency virus (HIV) infection may cause acquired immunodeficiency syndrome (AIDS). Although characterized by gradual destruction of cell-mediated (T cell) immunity, AIDS also affects humoral immunity and even autoimmunity through the central role of the CD4+ (helper) T lymphocyte in all immune reactions. The resulting immunodeficiency makes the patient susceptible to opportunistic infections, cancers, and other abnormalities that define AIDS.


·   HIV-1 retrovirus transmitted by contact with infected blood or body fluids

High-risk populations

·   Homosexual or bisexual men

·   I.V. drug users

·   Neonates of infected women

·   Recipients of contaminated blood or blood products

·   Heterosexual partners of persons in high-risk groups


The natural history of AIDS begins with infection by the HIV retrovirus, which is detectable only by laboratory tests, and ends with death. The HIV virus may enter the body by any of several routes involving the transmission of blood or body fluids; for example:

·   direct inoculation during intimate sexual contact

·   transfusion of contaminated blood or blood products

·   use of contaminated needles

·   transplacental or postpartum transmission.

HIV strikes helper T cells bearing the CD4+ antigen. Normally a receptor for major histocompatibility complex molecules, the antigen serves as a receptor for the retrovirus and allows it to enter the cell. Viral binding also requires the presence of a coreceptor on the cell surface. The virus may also infect CD4+ antigen-bearing cells of the GI tract, uterine cervix, and neuroglia.

Like other retroviruses, HIV copies its genetic material in a reverse manner compared with other viruses and cells. Through the action of reverse transcriptase, HIV produces DNA from its viral RNA. Transcription is often poor, leading to mutations, some of which make HIV resistant to antiviral drugs. The viral DNA enters the nucleus of the cell and is incorporated into the host cell's DNA, where it's transcribed into more viral RNA. If the host cell reproduces, it duplicates the HIV DNA along with its own and passes it on to the daughter cells. Thus, the host cell carries this information and, if activated, replicates the virus. Viral enzymes and proteases arrange the structural components and RNA into viral particles that move to the periphery of the host cell, where the virus buds and emerges from the host cell—free to infect other cells.

HIV replication may lead to cell death or the virus may become latent. HIV infection leads to profound pathology, either directly through destruction of CD4+ cells, other immune cells, and neuroglial cells, or indirectly through the secondary effects of CD4+ T-cell dysfunction and resulting immunosuppression.

Signs and symptoms


·   Mononucleosis-like syndrome, which may be attributed to flu or another virus; may remain asymptomatic for years

Symptomatic phase

·   Persistent generalized lymphadenopathy

·   Nonspecific symptoms, including weight loss, fatigue, night sweats

·   Fevers related to altered function of CD4+ cells, immunodeficiency, and infection of other CD4+ antigen-bearing cells

·   Neurologic symptoms

·   Opportunistic infection, cancer

Diagnostic test results

·   Laboratory studies reveal CD4+ T-cell count less than 200 cells/l and the presence of HIV antibodies


Antiretroviral agents

·   Protease inhibitors

·   Nucleoside reverse-transcriptase inhibitors

·   Nonnucleoside reverse-transcriptase inhibitors

Additional treatment

·   Immunomodulatory agents

·   Human granulocyte colony-stimulating growth factor

·   Anti-infective and antineoplastic agents

·   Supportive therapy, including nutritional support, fluid and electrolyte replacement therapy, pain relief, and psychological support

·   Treatment of opportunistic infections




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