Human immunodeficiency viral proteins

Inactivation and Removal of Viruses. In developing methods of plasma fractionation, the possibiHty of transmitting infection from human vimses present in the starting plasma pool has been recognized (4,5). Consequentiy, studies of product stabiHty encompass investigation of heat treatment of products in both solution (100) and dried (101) states to estabHsh vimcidal procedures that could be appHed to the final product. Salts of fatty acid anions, such as sodium caprylate [1984-06-17, and the acetyl derivative of the amino acid tryptophan, sodium acetyl-tryptophanate [87-32-17, are capable of stabilizing albumin solutions to 60°C for 10 hours (100) this procedure prevents the transmission of viral hepatitis (102,103). The degree of protein stabilization obtained (104) and the safety of the product in clinical practice have been confirmed (105,106). The procedure has also been shown to inactivate the human immunodeficiency vims (HIV) (107). 

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 vims (169). The formation of syncytia, normally observed when T-lymphoblastoid cell line (CEM) cells are cocultivated with human immunodeficiency vims (HlV-l)-infected T-ceU 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. 

Rossmann, M.G. Antiviral agents targeted to interact with viral capsid proteins and a possible application to human immunodeficiency virus. Proc. Natl. Acad. Sci. USA, 85 4625-4627, 1988. 

CarriUo A, Stewart KD, Sham HL, Norbeck DW, Kohlbrenner WE, Leonard JM, Kempf DJ, Molla A (1998) In vitro selection and characterization of human immunodeficiency virus type 1 variants with increased resistance to ABT-378, a novel protease inhibitor. J Virol 72 7532-7541 Chambers TJ, Nestorowicz A, Amberg SM, Rice CM (1993) Mutagenesis of the yellow fever virus NS2B protein effects on proteolytic processing, NS2B-NS3 complex formation, and viral replication. J Virol 67 6797-6807... 

Kobinger GP, Borsetti A, Nie Z, Mercier J, Daniel N, Gotthnger HG, Cohen A (1998) Virion-targeted viral inactivation of human immunodeficiency virus type 1 by using Vpr fusion proteins. J Virol 72 5441-5448... 

Okui N, Kobayashi N, Kitamura Y (1998) Production of uninfectious human immunodeficiency virus type 1 containing viral protein R fused to a single-chain antibody against viral integrase. J Virol 72 6960-6964... 

Madani N, Kabat D (2000) Cellular and viral specificities of human immunodeficiency virus type 1 vif protein. J Virol 74(13) 5982-5987... 

The proliferation of cytotoxic T-cells is markedly impaired upon infection with a newly discovered human immunodeficiency virus, designated HIV-V. The defect has been traced to the expression of a viral-encoded enzyme that inactivates a host-ceU nuclear protein required for DNA replication. Which protein is a potential substrate for the viral enzyme ... 

Replication of the human immunodeficiency virus (mV), the causative agent of AIDS, is susceptible to targeted interventions, because several virus-specific metabolic steps occur in infected cells (A). Viral RNA must first be transcribed into DNA, a step catalyzed by viral reverse transcriptase." Double-stranded DNA is incorporated into the host genome with the help of viral inte-grase. Under control by viral DNA, viral replication can then be initiated, with synthesis of viral RNA and proteins (including enzymes such as reverse transcriptase and integrase, and structural proteins such as the matrix protein lining the inside of the viral envelope). 

Heinzinger, N.K., Bukrinsky, M.I., Haggerty, S.A., Ragland, A.M., Kewalramani, V., Lee, M. et al. (1994) The Vpr protein of human immunodeficiency virus type 1 influences nuclear localization of viral nucleic acids in nondividing host cells. Proc. Natl. Acad. Sci. USA, 91, 7311-7315. 

Kichler, A., Pages, J.C., Leborgne, C., Druillennec, S., Lenoir, C., Coulaud, D. et al. (2000) Efficient DNA transfection mediated by the C-terminal domain of human immunodeficiency virus type 1 viral protein R. J. Virol., 74, 5424-5431. 

Human immunodeficiency virus (HIV) is a member of the retrovirus family, classified under the lentivirus genus. Retroviruses are enveloped RNA viruses, which contain a core of capsid proteins, viral RNA, and enzymes. All infectious retroviral virions contain an enzyme, reverse transcriptase, which catalyzes the formation of a complementary DNA strand from an RNA template. A double-stranded DNA copy of the viral RNA genome (proviral DNA) may then be integrated into and replicated with the host cell genome. 

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