Human immunodeficiency vims

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). 

Human Immunodeficiency Virus. Human immunodeficiency vims (HIV) causes Acquired Immunodeficiency Syndrome (AIDS), which has no cure. HIV infects the cells of the human immune system, such as T-lymphocytes, monocytes, and macrophages. After a long period of latency and persistent infection, it results in the progressive decline of the immune system, and leads to full-blown AIDS, resulting in death. 

Oxeta.nocins, Oxetanocia A (49), formerly oxetanocia, is the first naturally occurring oxetanose derivative and is isolated from Bacillus megaterium (1,145). It inhibits gram-positive bacteria, herpes vimses, and human immunodeficiency vims (HIV) (146). The chemical synthesis of (49) and several derivatives has been reported (147). 

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. 

RNA-dependent DNA polymerase (reverse transcriptase) oncomavims, human immunodeficiency vims (HIV)... 

Another dideoxypyrimidine nucleoside active against human immunodeficiency vims is 3 -azido-2/3 -dideoxyuridine [84472-85-5] (AZDU or CS-87, 64) C H N O. Since its synthesis, (167) CS-87 has been identified as a promising antiHIV agent (168) and is currentiy undergoing phase I clinical trials in patients with AIDS and AIDS-related complex. It appears to be less potent than AZT against HIV in a peripheral blood mononuclear (PBM) cell screening system and in MT-4 cell lines. This lower activity in PBM cells appears to be related to a lower affinity of CS-87 for the enzyme responsible for its initial phosphorylation (169). However, CS-87 has significantly lower toxicity on bone marrow cells than AZT (170) and penetration of the CNS as a 5 -dihydropyridine derivative. 

In 1983 the move to develop red cell substitutes intensified when it was recognized that the acquired immune deficiency syndrome (AIDS) could be transmitted by the blood-bome human immunodeficiency vims (HIV). Concern for the nation s blood supply followed. Since that time other retrovimses have been identified, efforts to screen blood not only for these agents but also for vimses that cause hepatitis have intensified, the indications for transfusion have been reevaluated, and the use of blood products has become much more efficient. More carehil screening of donors, testing of all donated units, and a general awareness in the donor population have all contributed to a decreased risk from transfusion-contracted AIDS. 

The family of apelin peptides is derived from a single gene, activate a single G-protein-coupled receptor and are substrates for the angiotensin converting enzyme-2 (ACE2). Apelins regulate cardiovascular function and fluid homeostasis. The apelin receptor also functions as a co-receptor for infection of CD4-positive cells by human immunodeficiency vims ( HIV). 

To circumvent this problem, vectors that are based on lentiviruses have been developed. In contrast to prototypic retroviruses, lentiviruses do not require cell division for integration. Gene-therapy vectors have been developed from a broad spectrum of lentiviruses including human immunodeficiency vims (HIV), simian and feline immunodeficiency vims as well as visna/maedi vims. The most widely used lentiviral vector system is based on HIV-1. These vectors can efficiently transduce a broad spectrum of dividing and nondividing cells including neurons, hepatocytes, muscle cells, and hematopoietic stem cells [1,2]. 

The human immunodeficiency vims (HIV) is the causative agent of the acquired immunodeficiency syndrome (AIDS). HIV is a retrovirus, whose replication includes the transcription of the single-stranded RNA genome into double stranded DNA (reverse transcription) and the covalent insertion of the DNA... 

Konstantinova P, de Vries W, Haasnoot J, Ter Brake O, de Haan P, Berkhout B (2006) Inhibition of human immunodeficiency vims type 1 by RNA interference using long-hairpin RNA. Gene Ther 13 1403-1413... 

Pearson L, Garcia J, Wu F, Modesti N, Nelson J, Gaynor R (1990) A transdominant tat mutant that inhibits tat-induced gene expression from the human immunodeficiency vims long terminal repeat. Proc Natl Acad Sci USA 87 5079-5083... 

Poznansky MC, La Vecchio J, Silva-Aiietta S, Porter-Brooks J, Brody K, Olszak IT, Adams GB, Ramstedt U, Marasco WA, Scadden DT (1999) Inhibition of human immunodeficiency vims replication and growth advantage of CD4+ T ceUs and monocytes derived from CD34-I- ceUs transduced with an intracellular antibody directed against human immunodeficiency vims type 1 Tat. Hum Gene Ther 10 2505-2514... 

Changes in human immunodeficiency vims type 1 Gag at positions 1449 and P453 are linked to I50V protease mutants in vivo and cause reduction of sensitivity to amprenavir and improved viral fitness in vitro. J Virol 76 7398-7406... 

Mammano F, Petit C, Clavel F (1998) Resistance-associated loss of viral fitness in human immunodeficiency vims type 1 phenotypic analysis of protease and gag coevolution in protease inhibitor-treated patients. J Virol 72 7632-7637... 

Budka H (1989) Human immunodeficiency virus (HlV)-induced disease of the central nervous system pathology and implications for pathogenesis. Acta Neuropathol 77(3) 225-236 Budka H (1991) Neuropathology of human immunodeficiency vims infection. Brain Pathol 1(3) 163-175... 

Byrn RA, Kiesshng AA (1998) Analysis of human immunodeficiency virus in semen indications of a genetically distinct virus reservoir. J Reprod Immunol 41(1-2) 161-176 Carr JM, Hocking H, Li P, Burrell CJ (1999) Rapid and efficient celL-to-ceU transmission of human immunodeficiency vims infection from monocyte-derived macrophages to peripheral blood lymphocytes. Virology 265(2) 319-329... 

There is much concern for the safety of personnel handling articles contaminated with pathogenic viruses such as hepatitis B virus (HB V) and human immunodeficiency vims (HIV) which causes acquired immune deficiency syndrome (AIDS). Some agents have been recommended for disinfection of HBV and HIV depending on the circumstances and level of contamination these are hsted in Table 10.4. Disinfectants must be able to treat rapidly and reliably accidental spills of blood, body fluids or secretions from HIV infected patients. Such spills may contain levels of HIV as high as lO" infectious units/ml. Recent evidence Irom the Medical Devices Agency evaluation of disinfectants against HIV indicated that few chemicals could destroy the vims in a... 

CYP. cytochrome P450 isoenzyme HIV, human immunodeficiency vims INR, International Normalized Ratio LFTs, liver function tests MAOI, monoamine oxidase inhibitor PT, prothrombin time TCA, tricyclic antidepressant. 

ART, antiretroviral therapy HIV, human immunodeficiency vims Ol, opportunistic infection. (Adapted from the DHHS Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents, April 7, 2005.)... 

Chabot DJ, Chen H, Dimitrov DS, Broder CC. N-Linked glycosylation ofCXCR4 Masks coreceptor function for CCR5-dependent human immunodeficiency vims type 1 isolates. J Virol 2000 74(9) 4404-4413. 

Kuhmann SE, Platt EJ, Kozak SL, Kabat D. Cooperation of multiple CCR5 coreceptors is required for infections by human immunodeficiency vims type 1. J Virol 2000 74(15) 7005-7015. 

Amara A, Vidy A, Boulla G, et al. G protein-dependent CCR5 signaling is not required for efficient infection of primary T lymphocytes and macrophages by R5 human immunodeficiency vims type 1 isolates. J Virol 2003 77(4) 2550-2558. 

Yoshida H, Koga Y, Moroi Y, Kimura G, Nomoto K. The effect of p561ck, a lymphocyte specific protein tyrosine kinase, on the syncytium formation induced by human immunodeficiency vims envelope glycoprotein. Int Immunol 1992 4(2) 233-242. 

Huang L, Bosch I, Hofmann W, Sodroski J, Pardee AB. Tat protein induces human immunodeficiency vims type 1 (HIV-1) coreceptors and promotes infection with both macrophage-tropic and T-lymphotropic HIV-1 strains. J Virol 1998 72(ll) 8952-8960. 

Kern, D., et al. (1996). An enhanced-sensitivity branched-DNA assay for quantification of human immunodeficiency vims type 1 RNA in plasma. J. Clin. Microbiol. 34,3196-3202. 

The problem of quality control in donor blood and blood products is of great importance for a health service in practice. Among infectious agents that contaminate blood, mention should be made of human immunodeficiency vims, hepatitis B and C vimses, and human cytomegalovirus (Ender, 2004 Mohr, 2000). In the past decade, the role of... 

Finally, it has been speculated that TNTs could represent a general mechanism for the intercellular spread of pathogens. In this respect, bacteria and retroviruses were seen to attach to the outer membrane and surf along the nanotubes towards connected cells, where they could be internalized (Onfelt et al., 2006 Sherer et al., 2007). Furthermore, the human immunodeficiency vims type 1 (HIV-1) was shown to move within nanotubes to infect connected cells (Sowinski et al., 2008). 

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