Genotypic analysis of plasma HIV-1 RNA after influenza vaccination of patients with previously undetectable viral loads

Kolber, Michael A.; Gabr, Abdel; Rosa, Abel De La; Glock, Jonathan A.; Jayaweera, Dushyantha; Miller, Nancimae; Dickinson, Gordon M.

doi:10.1097/00002030-200203080-00004

Cited by 35 publications

(25 citation statements)

References 22 publications

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“…In the population with human immunodeficiency virus (HIV) infection, there is no general consensus on the effects of influenza vaccination on viral loads or CD4 counts [86,87]. Nevertheless, vaccination of HIV-positive individuals has been found to induce protective antibodies in both early and advanced HIV disease irrespective of CD4 counts.…”

Section: Prophylaxis and Infectionmentioning

confidence: 99%

Influenza in the Intensive Care Unit

Oliveirã

Lee

Colice

2003

J Intensive Care Med

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Influenza remains an important epidemic viral infection. Thousands of deaths occur and billions of dollars are spent each year with influenza-related illnesses. Morbidity and mortality are largely attributed to respiratory complications that may require intensive care unit (ICU) admission. Medical and neonatal ICUs, transplant units, chronic-care wards, and nursing homes are at increased risk for nosocomial outbreaks of influenza, which are characterized by abrupt onset and rapid spread. In this article, the authors review the current concepts, recent advances, and management strategies in influenza-associated pneumonia. Pertinent issues to the critical care practitioner are discussed in detail.

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Section: Prophylaxis and Infectionmentioning

confidence: 99%

Influenza in the Intensive Care Unit

Oliveirã

Lee

Colice

2003

J Intensive Care Med

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“…Antibodies (or CTL) will alter extracellular concentrations of Env proteins, thus changing intracellular envelope concentrations once extracellular /intracellular Env concentrations equilibrate. Therefore, antibodies to heterologous envelope proteins – developing, for example, during immunization against other viruses or heterotypic co-infection – will reduce relative intracellular concentrations of variant envelope, favouring RNA pol :Env Wt interactions, thus enhancing replication and increasing mutation rates, a prediction confirmed in practice [38,56]. Contrariwise, antibodies to wild-type surface proteins – for example, during administration of anti-HBsAb following liver transplantation for HBV [63] – would reduce viral replication (Figure 6), as seen in practice.…”

Section: Discussionmentioning

confidence: 99%

Replicative Homeostasis: A fundamental mechanism mediating selective viral replication and escape mutation

Sallie¹

2005

Virol J

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Hepatitis C (HCV), hepatitis B (HBV), the human immunodeficiency viruses (HIV), and other viruses that replicate via RNA intermediaries, cause an enormous burden of disease and premature death worldwide. These viruses circulate within infected hosts as vast populations of closely related, but genetically diverse, molecules known as "quasispecies". The mechanism(s) by which this extreme genetic and antigenic diversity is stably maintained are unclear, but are fundamental to understanding viral persistence and pathobiology. The persistence of HCV, an RNA virus, is especially problematic and HCV stability, maintained despite rapid genomic mutation, is highly paradoxical. This paper presents the hypothesis, and evidence, that viruses capable of persistent infection autoregulate replication and the likely mechanism mediating autoregulation -Replicative Homeostasis -is described. Replicative homeostasis causes formation of stable, but highly reactive, equilibria that drive quasispecies expansion and generates escape mutation. Replicative homeostasis explains both viral kinetics and the enigma of RNA quasispecies stability and provides a rational, mechanistic basis for all observed viral behaviours and host responses. More importantly, this paradigm has specific therapeutic implication and defines, precisely, new approaches to antiviral therapy. Replicative homeostasis may also modulate cellular gene expression.

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“…Several studies have examined replication of HIV after immune stimulation with influenza vaccine or other antigens, noting viral load levels in blood and PBMCs and effects on lymphocyte subpopulation changes in peripheral blood [O'Brien et al, 1995;Glesby et al, 1996;Stanley et al, 1996;Kolber et al, 2002;Skiest and Machala, 2003]. Kolber et al [2002] reported that a small subset of patients had increased HIV loads following influenza vaccination and that these could be associated with mutational changes in the RT region of the HIV genome.…”

Section: Discussionmentioning

confidence: 99%

“…Kolber et al [2002] reported that a small subset of patients had increased HIV loads following influenza vaccination and that these could be associated with mutational changes in the RT region of the HIV genome. Similarly, Stanley et al [1996] reported that HIV levels rose transiently following stimulation with the recall antigen tetanus toxoid.…”

Section: Discussionmentioning

confidence: 99%

Blood levels of TT virus following immune stimulation with influenza or hepatitis B vaccine

Maggi¹,

Tempestini²,

Lanini³

et al. 2004

Journal of Medical Virology

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Torque Teno virus (TTV) has been demonstrated to be present persistently in the blood of healthy individuals without evidence that it causes any disease process. The levels of TTV vary in patients co-infected with other viruses and there has been considerable speculation as to whether TTV contributes to pathogenesis by other viruses or if the varying levels might be related to immune activation in the host. In the present study, the load of TTV was examined in plasma and peripheral blood mononuclear cells (PBMCs) following immunization of subjects with either influenza (a recall antigen) or hepatitis B virus (HBV) (a new antigenic exposure). The results overall did not indicate a significant change in TTV titers over a 90 day observation period; however, when TTV genogroup was taken into consideration there was an increase in viral load in plasma at some time points for subjects persistently infected with genogroup 3. While this was observed in both influenza and HBV immunized subjects, the effect was more profound in HBV vaccination. Thus, it appears that exposure to a new antigen rather than a recall antigen may stimulate TTV replication more effectively. The data further suggest that investigating the interactions between TTV and its host might require to examine specifically each TTV genogroup separately in order to determine if certain TTV types have any role in disease pathogenesis.

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Genotypic analysis of plasma HIV-1 RNA after influenza vaccination of patients with previously undetectable viral loads

Cited by 35 publications

References 22 publications

Influenza in the Intensive Care Unit

Influenza in the Intensive Care Unit

Replicative Homeostasis: A fundamental mechanism mediating selective viral replication and escape mutation

Blood levels of TT virus following immune stimulation with influenza or hepatitis B vaccine

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