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Influenza A H5N1 and HIV co-infection: case report

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  • Influenza A H5N1 and HIV co-infection: case report

    Case report
    Influenza A H5N1 and HIV co-infection: case report

    Annette Fox email, Peter Horby email, Nguyen Hong Ha email, Le Nguyen Minh Hoa email, Nguyen Tien Lam email, Cameron Simmons email, Jeremy Farrar email, Nguyen Van Kinh email and Heiman Wertheim email

    BMC Infectious Diseases 2010, 10:167doi:10.1186/1471-2334-10-167
    Published: 14 June 2010
    Abstract (provisional)

    Background

    The role of adaptive immunity in severe influenza is poorly understood. The occurrence of influenza A/H5N1 in a patient with HIV provided a rare opportunity to investigate this.
    Case presentation

    A 30-year-old male was admitted on day 4 of influenza-like-illness with tachycardia, tachypnea, hypoxemia and bilateral pulmonary infiltrates. Influenza A/H5N1 and HIV tests were positive and the patient was treated with Oseltamivir and broad-spectrum antibiotics. Initially his condition improved coinciding with virus clearance by day 6. He clinically deteriorated as of day 10 with fever recrudescence and increasing neutrophil counts and died on day 16. His admission CD4 count was 100/ul and decreased until virus was cleared. CD8 T cells shifted to a CD27+CD28- phenotype. Plasma chemokine and cytokine levels were similar to those found previously in fatal H5N1.
    Conclusions

    The course of H5N1 infection was not notably different from other cases. Virus was cleared despite profound CD4 T cell depletion and aberrant CD8 T cell activation but this may have increased susceptibility to a fatal secondary infection.

    Background The role of adaptive immunity in severe influenza is poorly understood. The occurrence of influenza A/H5N1 in a patient with HIV provided a rare opportunity to investigate this. Case Presentation A 30-year-old male was admitted on day 4 of influenza-like-illness with tachycardia, tachypnea, hypoxemia and bilateral pulmonary infiltrates. Influenza A/H5N1 and HIV tests were positive and the patient was treated with Oseltamivir and broad-spectrum antibiotics. Initially his condition improved coinciding with virus clearance by day 6. He clinically deteriorated as of day 10 with fever recrudescence and increasing neutrophil counts and died on day 16. His admission CD4 count was 100/μl and decreased until virus was cleared. CD8 T cells shifted to a CD27+CD28- phenotype. Plasma chemokine and cytokine levels were similar to those found previously in fatal H5N1. Conclusions The course of H5N1 infection was not notably different from other cases. Virus was cleared despite profound CD4 T cell depletion and aberrant CD8 T cell activation but this may have increased susceptibility to a fatal secondary infection.

  • #2
    Re: Influenza A H5N1 and HIV co-infection: case report

    Some more excepts from this article on this patient from Vietnam:

    Background
    Influenza A/H5N1 infection is characterized by high viral loads, overproduction of pro-inflammatory cytokines and chemokines, direct lung tissue destruction, pulmonary oedema and extensive inflammatory infiltration. The prevailing view is that alveoloar dmage is the primary pathology leading to acute respiratory distress, multiple organ dysfunction syndomre and death. Likewise, 2009 H1N1 infection can cause acute respiratory distress syndrome and death in previously healthy young adults very similar to the clinical syndrome seen in H5N1.

    Case Presentation
    Three days prior to illness onset he had slaughtered, prepared and consumed a duck that was the last survivor of a household flock of ten birds, which had died over the preceding week.

    Conclusions
    The patient maintained substantial numbers of peripheral CD8 T cells and a large fraction became activated, but the concomitant shift to a CD27+CD28- phenotype raises doubts about their antiviral function. This phenotype is associated with CD8 T cells that proliferate but lack cytotoxic function and accumulate in progressive HIV infection.

    There has been no conclusive report of secondary infection accompanying H5N1 whereas secondary pneumonia may have caused a considerable fraction of the deaths from the highly pathogenic 1918 H1N1 strain and the current H1N1 2009 strain. Findings in this patient including recrudescence of fever, rising CRP levels and neutrophilia were consistent with a secondary infection despite being treated with broad-spectrum antibiotics. A. fumigatus was detected in a tracheal aspirate suggestive of invasive pulmonary aspergillosis.

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