Otolaryngologic manifestations of HIV infection

B Viswanatha

Abstract


HIV is a retrovirus on the Lentivirus subfamily. The virus binds to the CD4 receptor on the T helper lymphocytes. Fusion of the viral and cell membranes allows entry of the viral core into the cell. The reverse transcriptase enzyme, a protein carried by the virus that allows transcription of ribonucleic acid (RNA) into deoxyribonucleic acid, then mediates transcription of the viral RNA genome into viral DNA. Viral integrase then facilitates incorporation of the viral DNA into the host genome. The viral DNA is then transcribed into multiple RNA copies by the host cell. This newly created RNA is translated into viral proteins. Translation of the viral RNA sequences results in protein precursors that undergo proteolytic processing by a viral protease that liberates the functional viral proteins [1, 2].

As the virus infects and damages helper T cells, both humoral and cell-mediated immunity are impaired. Defective chemotaxis and phagocytosis causes increased vulnerability to infections such as candidiasis and toxoplasmosis. A lack of T-cell stimulation of B cells results in decreased immunoglobulin production and a vulnerability to encapsulated organisms such as Streptococcus pneumoniae and other bacteria. These problems are compounded by impaired neutrophil function [2].


Full Text: PDF DOI: 10.5430/jhm.v2n2p33

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Journal of Hematological Malignancies
ISSN 1925-4024 (Print)   ISSN 1925-4032 (Online)
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