Etiology

HIV exists in two distinct forms, HIV-1 and HIV-2. HIV-2 appears to be a less virulent form of the virus that is usually associated with a slower clinical course. Unfortunately, 99.9% of HIV-infected individuals within the United States are infected with HIV-1 (10). HIV has a remarkable capacity for both replication and mutation. HIV produces an estimated 1010 new particles daily while generating one mutation per genome per cycle (11).

HIV may be further classified as syncytium inducing (SI) or non-syncytium inducing (NSI) (12). Syncytia are fusions of cells into large multinucleated cells. This phenomenon has been observed in other viral diseases including herpesvirus infections, measles, parainfluenza, and mumps. It occurs in HIV when infected cells expressing viral proteins bind to other cells expressing CD4+ receptors, such as T lymphocytes. Whether or not a virus is SI depends upon its chemokine receptors. Patients with SI virus appear to have a more rapid disease progression (13).

Once HIV is transmitted and gains entry to the bloodstream, it seeks out CD4+ cells through receptor-mediated identification and entry (Fig. 1) (14). CD4+ cells, named for their CD4+ receptors, play an integral role in the overall modulation of the immune system. With damage to CD4+ cells, the immune system is rendered dysfunctional. Within the host CD4+ cells, the virus will prepare to manufacture the necessary viral components for replication. HIV is classified as a retrovirus; therefore, its endogenous genetic material is RNA, unlike the human endogenous genetic material, which consists of DNA (5). Retroviruses transcribe RNA to DNA then back to RNA; RNA is then eventually translated into viral proteins. The transcription of RNA to DNA is accomplished by a retrovirus-exclusive enzyme known as reverse transcrip-tase (14).

Once HIV has catalyzed the conversion of viral RNA to viral DNA, the DNA must be integrated into human DNA. This is accomplished via the viral enzyme integrase and is a necessary step in the replication cycle because HIV lacks the cellular machinery for the transcription of DNA (14). In effect, the virus takes advantage of the host CD4+ cell, which will inadvertently aid in HIV replication by transcribing the integrated piece of viral DNA into viral RNA.

After viral DNA is transcribed and viral RNA is translated, viral proteins are manufactured (Fig. 1). These proteins are polyproteins that require catalytic cleavage by HIV protease enzymes for activation. Upon activation of these proteins, HIV will assemble itself and depart from the host cell (14). This new virion will then infect another CD4+ cell and repeat the replication cycle. The processes involved in the release of the new HIV virions result in CD4+ cell death.

As CD4+ cell counts decline (normal 800-1000 cells/mm3), immune system function is adversely affected, and the patient is at risk for the development of opportunistic infections such as tuberculosis, PCP, cytomegalovirus, and toxoplasmosis (14). Death is usually not a result of HIV disease itself but rather occurs from the secondary opportunistic infections or malignancies that develop.

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