Literature DB >> 8092178

HIV-1 infection despite immediate combination antiviral therapy after infusion of contaminated white cells.

D L Palmer1, B L Hjelle, C A Wiley, S Allen, W Wachsman, R G Mills, L E Davis, T L Merlin.   

Abstract

We present a sixth human case in which primary human immunodeficiency virus (HIV-1) infection occurred, despite antiretroviral prophylaxis, after accidental inoculation of infected blood. In the prior five instances, variables such as large virus dose, late administration of antivirals, viral resistance to zidovudine, and pre-existent immunosuppression, may have played a role in the treatment failure. In this case, high-dosage oral zidovudine was given within minutes of the accident and replaced 2 1/2 days later with interferon alpha and dideoxyinosine (ddl). Despite aggressive treatment, HIV-1 infection was demonstrated in blood, spleen, and brain tissue at autopsy 16 days later. Of the tissues studied, detection of HIV-1 was most prominent in the spleen. Double-label immunocytochemistry confirmed the morphologic impression that while some of the infected spleen cells were CD3-positive T cells, the majority were macrophages. Thus, current single or dual (zidovudine, ddl-interferon) therapies for accidental HIV-1 inoculation may not be effective in preventing early infection. Further trials in animals appear warranted to evaluate protection by other strategies, such as passive immunity or combinations of agents that penetrate the brain and attack HIV-1 viral replication at differing sites.

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Year:  1994        PMID: 8092178     DOI: 10.1016/0002-9343(94)90012-4

Source DB:  PubMed          Journal:  Am J Med        ISSN: 0002-9343            Impact factor:   4.965


  8 in total

1.  Evidence that high-dosage zidovudine at time of retrovirus exposure reduces antiviral efficacy.

Authors:  L E Mathes; K A Hayes; G Kociba
Journal:  Antimicrob Agents Chemother       Date:  1996-09       Impact factor: 5.191

2.  Transcriptional Regulation of CXCL5 in HIV-1-Infected Macrophages and Its Functional Consequences on CNS Pathology.

Authors:  Debjani Guha; Cynthia R Klamar; Todd Reinhart; Velpandi Ayyavoo
Journal:  J Interferon Cytokine Res       Date:  2014-12-23       Impact factor: 2.607

3.  RON receptor tyrosine kinase, a negative regulator of inflammation, is decreased during simian immunodeficiency virus-associated central nervous system disease.

Authors:  Daniele C Cary; Janice E Clements; Andrew J Henderson
Journal:  J Immunol       Date:  2013-09-16       Impact factor: 5.422

4.  CD40-CD40 ligand interactions in human microglia induce CXCL8 (interleukin-8) secretion by a mechanism dependent on activation of ERK1/2 and nuclear translocation of nuclear factor-kappaB (NFkappaB) and activator protein-1 (AP-1).

Authors:  Teresa G D'Aversa; Eliseo A Eugenin; Joan W Berman
Journal:  J Neurosci Res       Date:  2008-02-15       Impact factor: 4.164

5.  Enteric ganglionitis in rhesus macaques infected with simian immunodeficiency virus.

Authors:  Marlene S Orandle; Ronald S Veazey; Andrew A Lackner
Journal:  J Virol       Date:  2007-03-28       Impact factor: 5.103

Review 6.  The role of host genetics in the susceptibility for HIV-associated neurocognitive disorders.

Authors:  Andrew J Levine; Elyse J Singer; Paul Shapshak
Journal:  AIDS Behav       Date:  2008-02-09

7.  Region-specific distribution of human immunodeficiency virus type 1 long terminal repeats containing specific configurations of CCAAT/enhancer-binding protein site II in brains derived from demented and nondemented patients.

Authors:  Tricia H Burdo; Suzanne Gartner; David Mauger; Brian Wigdahl
Journal:  J Neurovirol       Date:  2004       Impact factor: 2.643

8.  Neuronal apoptosis by HIV-1 Vpr: contribution of proinflammatory molecular networks from infected target cells.

Authors:  Debjani Guha; Pruthvi Nagilla; Carrie Redinger; Alagarsamy Srinivasan; Gerald P Schatten; Velpandi Ayyavoo
Journal:  J Neuroinflammation       Date:  2012-06-22       Impact factor: 8.322

  8 in total

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