Summary This report updates U.S. Public Health Service recommendations for the management of health-care personnel (HCP) who have occupational exposure to blood and other body fluids that might contain human immunodeficiency virus (HIV). Although the principles of exposure management remain unchanged, recommended HIV postexposure prophylaxis (PEP) regimens have been changed. This report emphasizes adherence to HIV PEP when it is indicated for an exposure, expert consultation in management of exposures, follow-up of exposed workers to improve adherence to PEP, and monitoring for adverse events, including seroconversion. To ensure timely postexposure management and administration of HIV PEP, clinicians should consider occupational exposures as urgent medical concerns.

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Updated U.S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis.

During the past 6 years, there have been substantial advances in our understanding of human immunodeficiency virus 1 and other viruses, such as hepatitis B virus and hepatitis C virus, that cause chronic infection. The use of mathematical modelling to interpret experimental results has made a significant contribution to this field. Mathematical modelling is also improving our understanding of T-cell dynamics and the quantitative events that underlie the immune response to pathogens.

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Modelling viral and immune system dynamics

Disclosed herein are small interfering RNAs (siRNAs), and vectors encoding one or more siRNAs (including short hairpin siRNAs), that are sufficiently homologous to a portion of the HIV genome to mediate RNA interference in vivo. Also disclosed are methods wherein siRNAs, or vectors encoding siRNAs, are administered to prevent or inhibit HIV infection in a subject, cell or tissue. Knockout and/or knockdown cells or organisms are also disclosed that utilize the siRNAs or vectors of the present invention.

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Modulation of hiv replication by rna interference

Early steps of infection by HIV-1 involve entry of the viral core into cells, reverse transcription to form the linear viral DNA, and integration of that DNA into a chromosome of the host. The unintegrated DNA can also follow non-productive pathways, in which it is circularized by recombination between DNA long-terminal repeats (LTRs), circularized by ligation of the DNA ends or degraded. Here we report quantitative methods that monitor formation of reverse transcription products, two-LTR circles and integrated proviruses. The integration assay employs a novel quantitative form of Alu-PCR that should be generally applicable to studies of integrating viruses and gene transfer vectors.

A quantitative assay for HIV DNA integration in vivo.

▪ Abstract A viral reservoir is a cell type or anatomical site in association with which a replication-competent form of the virus accumulates and persists with more stable kinetic properties than the main pool of actively replicating virus. This article reviews several cell types and anatomical sites proposed as potential reservoirs for HIV-1. It is now clear that HIV-1 persists in a small reservoir of latently infected resting memory CD4+ T cells, which shows minimal decay even in patients on highly active antiretroviral therapy (HAART). The persistence of virus in this reservoir is consistent with the biology of these cells and the long-term persistence of immunologic memory. The viral replication that continues in patients on suppressive HAART may also contribute to the stability of this reservoir. There may be other reservoirs, but the latent reservoir in resting CD4+ T cells appears to be sufficient to guarantee lifetime persistence of HIV-1 in the majority of patients on current HAART regimens, and...

The challenge of viral reservoirs in HIV-1 infection.

Treatment of HIV-1-infected individuals with a combination of anti-retroviral agents results in sustained suppression of HIV-1 replication, as evidenced by a reduction in plasma viral RNA to levels below the limit of detection of available assays. However, even in patients whose plasma viral RNA levels have been suppressed to below detectable levels for up to 30 months, replication-competent virus can routinely be recovered from patient peripheral blood mononuclear cells and from semen. A reservoir of latently infected cells established early in infection may be involved in the maintenance of viral persistence despite highly active anti-retroviral therapy. However, whether virus replication persists in such patients is unknown. HIV-1 cDNA episomes are labile products of virus infection and indicative of recent infection events. Using episome-specific PCR, we demonstrate here ongoing virus replication in a large percentage of infected individuals on highly active anti-retroviral therapy, despite sustained undetectable levels of plasma viral RNA. The presence of a reservoir of 'covert' virus replication in patients on highly active anti-retroviral therapy has important implications for the clinical management of HIV-1-infected individuals and for the development of virus eradication strategies.

Persistence of episomal HIV-1 infection intermediates in patients on highly active anti-retroviral therapy.

The availability of sensitive assays for plasma HIV viral load and the trend toward earlier and more aggressive treatment of HIV infection have led to the inappropriate use of these assays as prima...

http://reducetheburden.org/wp-content/uploads/2009/03/316-misdiagnosis-by-vl.pdf

Brian J. Mady

Papers

Persistence of episomal HIV-1 infection intermediates in patients on highly active anti-retroviral therapy.

Misdiagnosis of HIV infection by HIV-1 plasma viral load testing: a case series

Adult Group B Streptococcal Disease