Human immunodeficiency vims infection

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... 

Palella FJ, Delaney KM, Moorman AC, loveless MO, Fuhrer J, Satten GA, Aschman DJ, Holmbeig SD Declining morbidity and mortality among patients with advanced human immunodeficiency vims infection. N EngJ J Med 1998 338 853-860. 

Cysique LA, Mai uff P, Brew BJ (2004) Pi evalence and pattern of neui opsychological impaimient in human immunodeficiency vims-infected/acquired immunodeficiency syndrome (HIV/AIDS) padents across pre- and post-highly acdve andreti oviral dierapy eras A combined study of two cohorts. J Neur ovirol 10 350—357. 

Bndka H (1991) Nenropathology of human immunodeficiency vims infection. Brain Pathol 1 163-175. 

Stout JC, EUis RJ, Jemigan TL, Archibald SL, Abramson 1, Wolfson T, McCutchan JA, Wallace MR, Atkinson JH, Grant I, HIV Neurobe-havioral Research Center Group (1998) Progressive cerebral volume loss in human immunodeficiency vims infection A longitudinal volumetric magnetic resonance imaging study. Arch Neurol 55 161-168. 

Kline MW, Calles NR, Simon C, Schwarzwald H. Pilot study of hydroxyurea in human immunodeficiency vims-infected children receiving didanosine and/or stavudine. Pediatr Infect Dis J 2000 19(ll) 1083-6. 

Wormser GP, Horowitz HW, Duncanson FP, Forseter G, Javaly K, Alampur SK, Gilroy SA, Lenox T, Rappaport A, Nadehnan RB. Low-dose intermittent trimethoprim-sulfamethoxazole for prevention of Pneumocystis carinii pneumonia in patients with human immunodeficiency vims infection. Arch Intern Med 1991 151(4) 688-92. 

Collier AC, Bozzette S, Coombs RW, Cansey DM, Schoenfeld DA, Spector SA, Pettinelh CB, Davies G, Richman DD, Leedom JM, et al. A pilot stndy of low-dose zidovudine in human immunodeficiency vims infection. N Engl J Med 1990 323(15) 1015-21. 

Ippolito, G. Puro, V. De Carli, G. The Italian study group on occupational risk of HIV infection. The risk of occupational human immunodeficiency vims infection in health care workers. Arch. Intern. Med. 1993, 153, 1451-1458. 

Telzak EE. Tuberculosis and human immunodeficiency vims infection. Med Clin North Am 1997 81 345-360. 

Mastroianni CM, d Ettorre G, Forcina G, Lichtner M, Mengoni F, D Agostino C, Corpolongo A, Massetti AP, Vullo V Interleukin-15 enhances neutrophil functional activity in patients with human immunodeficiency vims infection. Blood 2000 96 1979-1984. 

Goldenberg, D. M. Chang, C. H. Rossi, E. A. McBride, W. J. Methods and compositions for treatment of human immunodeficiency vims infection with conjugated antibodies or antibody fragments. U.S. Pat. Appl. Publ. US 2007264265, 2007 Chem. Abstr. 2007, 147, 534630. 

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. 

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. 

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). 

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... 

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.)... 

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. 

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. 

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). 

The disease known as acquired immune deficiency S5mdrome (AIDS) was first reported in 1981, and the virus that causes it continues to create formidable challenges to the biomedical research and public health communities around the world. Globally, about 14,000 individuals are newly infected daily with one of the nine known subtypes of human immunodeficiency vims (HIV) that cause AIDS. Cumulatively, as of the year 2004, the vims has infected more than 70 million individuals, killing about 30 million and leaving another 40 million with an infection that is ultimately fatal. More than 90% of these infections have occurred in the developing world, where access to antiretroviral therapy is minimal. 

Bukrinsky, M.I., Sharova, N., McDonald, T.L., Pushkarskaya, T., Tarpley, W.G. and Stevenson, M. (1993) Association of integrase, matrix, and reverse transcriptase antigens of human immunodeficiency vims type 1 with viral nucleic acids following acute infection. Proc. Natl. Acad. Sci. USA, 90, 6125-6129. 

In the past, various serendipitous discoveries have capitalized on the differential expression of enzymes by host and viral infected cells. For example, the prodrug Acyclovir, used widely for the treatment of herpes simplex and herpes zoster infections, is selectively activated through phosphorylation by viral thymidine kinase to acyclovir monophosphate which is then converted to the triphosphate, which inhibits DNA polymerase, by host cellular enzymes. Similarly several 2, 3 -dideoxynucleoside analogs such as Zidovudine (azidothymidine, AZT) and 2, 3 -didehydro-3 -deoxythymidine (D4T) have potent antiviral activity against human immunodeficiency vims (HIV). These compounds are selectively phosphoiylated intracellularly to the 5 -triphosphate derivatives which inhibit the viral reverse transcriptase. 

There was a significantly increased prevalence of infection in the infants of cocaine-using mothers. Hepatitis was 42 times more common, syphilis was 15 times as common, and human immunodeficiency vims positivity was 16 times more common (although the overall prevalence was only 0.1%). Exposure to cocaine increased the likelihood of involvement with social services such as child protection agencies. 

Vlietinck, A. J. Bmyne, T. D. Apers, S. Pieters, L. A. Plant-derived leading compounds for chemotherapy of human immunodeficiency vims (HIV) infection. Planta Medico, 1998, 64 97-109. 

Korting HC, Schaller M, Eder G, Hamm G, Bohmer U, Hube B Effects of the human immunodeficiency vims (HIV) proteinase inhibitors Saquinavir and Indinavir on in vitro activities of secreted aspartyl proteinases of Candida albicans isolates from HIV-infected patients. Antimicrob Agents Chemother 1999 43 2038-2042. 

Cassone A, De Bemardis F, Torosantucci A, Tacconelli E, Tumbarello M, Cauda R In vitro and in vivo anticandidal activity of human immunodeficiency vims protease inhibitors. J. Infect Dis 1999 180 448 53. 

Paquette, J.S., Fortin, J.F., Blanchard, L. and Tremblay, M.J. (1998) Level of ICAM-1 surface expression on vims producer cells influences both the amount of virion-bound host ICAM-1 and human immunodeficiency vims type 1 infectivity. J. Virol. 72, 9329-9336. 

Tardif, MR. and Tremblay, M. J. (2003) Presence of host ICAM-1 in human immunodeficiency vims type 1 virions increases productive infection of CD4+ T lymphocytes by favoring cytosolic delivery of viral material. J. Virol. 77, 12299-12309. 

Harouse JM, CoUman RG, Gonzalez-Scarano F. Human immunodeficiency vims type 1 infection of SK-N-MC cells domains of gpl20 involved in entry into a CD4-negative, galactosyl ceramide/3 -sulfogalactosyl ceramide-positive cell line. J. Virol. 1995 69 7383-7390. 

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