Human immunodeficiency virus infection mechanisms

Beach JW. Chemotherapeutic agents for human immunodeficiency virus infection mechanism of action, pharmacokinetics, metabolism, and adverse reactions. Clin Ther 1998 20 2-25. 

Harbol AW, Liesveld JL, Simpson-Haidaiis PJ, Abboud CN (1994) Mechanisms of cytopenia in human immunodeficiency virus infection. Blood Rev 8(4) 241-251 Harris RS, Sheehy AM, Craig HM, Malim MH, Neuberger MS (2003) DNA deamination not just a trigger for antibody diversification but also a mechanism for defense against retroviruses. Nat Immunol 4(7) 641-643... 

Perea S, JL Lopez-Ribot, WR Kirkpatrick, RK McAtee, RA Santillan, M Martinez, D Calabrese, D Sanglard, TP Patterson (2001) Prevalence of molecular mechanisms of resistance to azole antifungal agents in Candida albicans strains displaying high-level fluconazole resistance isolated from human immunodeficiency virus-infected patients. Antibicrob Agents Chemother 45 2676-2684. 

Neuropathy in human immunodeficiency virus infection has many causes. Multiple mechanisms cause neuropathy in patients with HIV. An immune-mediated, Guillain-Barre-like syndrome (see below) may occur at the time of HIV seroconversion. Later in the course of infection, patients may present with mononeuropathy multiplex, sometimes as a consequence of vasculitis associated with coinfection with hepatitis C. Distal sensory-autonomic axonal polyneuropathy may develop in patients with more advanced HIV, either as a consequence of high titers of HIV itself or of the neurotoxicity of antiretroviral drugs [18,19],... 

A.S. Fauci. 1988. The human immunodeficiency virus Infectivity and mechanisms of pathogenesis Science 239 617-622. (PubMed)... 

Fauci, A.S. The human immunodeficiency virus infectivity and mechanisms of pathogenesis. Science 239(4840), 617-622 (1988)... 

Li, X. L., Moudgil, T., Vinters, H. V., and Ho, D. D. (1990) CD4-independent, productive infection of a neuronal cell line by human immunodeficiency virus type 1. J. Virol. 64,1383-1387. Moses, A. V., Bloom, F. E., Pauza, C. D., and Nelson, J. A. (1993) Human immunodeficiency virus infection of human brain capillary endothelial cells occurs via a CD4/galactosy Iceramide-independent mechanism. Proc. Natl. Acad. Sci. USA 90,10474—10478. 

Cannabinoids have antiemetic activity when used alone or in combination with other antiemetics.5 Dronabinol and nabilone are commercially available oral formulations used for preventing and treating refractory CINV.5,10 Dronabinol is also used to treat anorexia and weight loss associated with human immunodeficiency virus (HIV) infection. Cannabinoids are thought to exert their antiemetic effect centrally, although the exact mechanism of action is unknown.1,10 Sedation, euphoria, hypotension, ataxia, dizziness, and vision difficulties can occur with cannabinoids. 

This outline is not exhaustive. For example there is an increasing awareness of the role played by infection with the human immunodeficiency virus while infiltration of the marrow with fibrous tissue or tumour cells will decrease production. In much the same way massive splenomegaly, so common in tropical Africa, sequesters significant volumes of red cells while malarial infection results in their accelerated breakdown. In some cases defects are multifactorial as in chronic lymphocytic leukaemia where infiltration decreases production, splenomegaly traps large amounts of blood while immune mechanisms lead to shortened survival or haemolysis. 

Exploded view of the human immunodeficiency virus. It is an RNA (retrovirus) virus that contains surface proteins composed of a knoblike glycoprotein (gpl20) linked to a transmembrane stalk (gp41). These surface proteins are the infective mechanisms that allow the virus to bind to CD4 proteins of cells, such as T4 lymphocytes and monocytes. 

The mechanism of inhibition has not been characterized, but it is probably related to the ionophoretic properties of these antibiotics. Monensin has been shown to inhibit the intracellular transport of viral membrane proteins of cells infected with Semliki Forest virus (169). The formation of syncytia, normally observed when T-lymphoblastoid cell line (CEM) cells are cocultivated with human immunodeficiency virus (HlV-l)-infected T-cell leukemia cell line (MOLT-3) cells, was significantly inhibited in the presence of monensin (170). This observation suggests that the viral glycoproteins in the treated cells were not transported to the cell surface from the Golgi membrane. 

Acid-labile formylation of A-terminal proline of HIV-1 was found by proteomics. The role of formylation of human immunodeficiency virus type 1 p24 is unclear so far, but it is surmised that the acid-labile formylation of H1V-1lav-i p24 may play a critical role in the formation of the HIV-1 core for conferring HlV-1 infectivity. Furthermore, peptide-mass fingerprinting data suggest that two isoforms of cyclophilin A (CyPA), one with an isoelectric point (pi) of 6.40 and one with a pi of 6.53, are inside the viral membrane and another isoform with a pi of 6.88 is outside the viral membrane, and that the CyPA isoform with a pi of 6.53 is V-acetylated. The mechanisms that permit the redistribution of CyPA on the viral surface have not yet been clarified, but it is surmised that the CyPA isoform with a pi of 6.88 may play a critical role in the attachment of virions to the surface of target cells, and both the CyPA isoforms with pis of 6.40 and 6.53 may regulate the conformation of the HlV-1 capsid protein. 

Gordon CJ, Muesing MA, Proudfoot AE, Power CA, Moore JP, Trkola A. Enhancement of human immunodeficiency virus type 1 infection by the CC-chemokine RANTES is independent of the mechanism of virus-ceU fusion. J Virol 1999 73 684-694. 

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