Accumulation of activated CD4 super(+) lymphocytes in the lung of individuals infected with HIV accompanied by increased virus production in patients with secondary infections
The lung is continuously exposed to infectious and non-infectious agents causing cell activation. Activated cells in the lung such as antigen-presenting cells which harbour HIV may favour this organ as a site for virus production. To test this hypothesis, cells from blood and bronchoalveolar lavage...
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Veröffentlicht in: | Clinical and experimental immunology 1995-01, Vol.102 (2), p.231-237 |
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Sprache: | eng |
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Zusammenfassung: | The lung is continuously exposed to infectious and non-infectious agents causing cell activation. Activated cells in the lung such as antigen-presenting cells which harbour HIV may favour this organ as a site for virus production. To test this hypothesis, cells from blood and bronchoalveolar lavage (BAL) of HIV-infected patients and healthy controls were obtained and the activation of the cells were analysed by measuring the expression of IL-2 receptor, HLA-DR and VLA-1. The HIV-infected individuals were subdivided into 'lung symptomatic' or 'lung asymptomatic' patients, depending on the presence or absence of secondary lung diseases besides HIV. All HIV-infected individuals demonstrated a decreased number of CD4 super(+) lymphocytes in blood; however, normal numbers of these cells were found in BAL. The activation state of CD4 super(+) and CD8 super(+) T lymphocytes in blood and BAL was higher in lymphocytes from HIV-infected patients compared with controls. The activation state was highest in the lung symptomatic group. Lung symptomatic patients and lung asymptomatic patients with extrapulmonary infections had increased levels of free virus in plasma. Four out of four individuals without or with only low amounts of cell-free HIV in plasma belonged to the symptom-free subgroup. These results suggest that microorganisms other than HIV may promote viral replication via antigen-driven accumulation and activation of CD4 super(+) cells in the lung or other organs, and thus may be responsible for the loss of helper T cells and the progression of the disease. |
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ISSN: | 0009-9104 |