ACCUMULATION OF ACTIVATED CD4(+) LYMPHOCYTES IN THE LUNG OF INDIVIDUALS INFECTED WITH HIV ACCOMPANIED BY INCREASED VIRUS PRODUCTION IN PATIENTS WITH SECONDARY INFECTIONS

Citation
M. Franchini et al., ACCUMULATION OF ACTIVATED CD4(+) LYMPHOCYTES IN THE LUNG OF INDIVIDUALS INFECTED WITH HIV ACCOMPANIED BY INCREASED VIRUS PRODUCTION IN PATIENTS WITH SECONDARY INFECTIONS, Clinical and experimental immunology, 102(2), 1995, pp. 231-237
Citations number
40
Categorie Soggetti
Immunology
ISSN journal
00099104
Volume
102
Issue
2
Year of publication
1995
Pages
231 - 237
Database
ISI
SICI code
0009-9104(1995)102:2<231:AOACLI>2.0.ZU;2-T
Abstract
The lung is continuously exposed to infectious and non-infectious agen ts causing cell activation. Activated cells in the lung such as antige n-presenting cells which harbour HIV may favour this organ as a site f or virus production. To test this hypothesis, cells from blood and bro nchoalveolar lavage (BAL) of HIV-infected patients and healthy control s were obtained and the activation of the cells were analysed by measu ring the expression of IL-2 receptor, HLA-DR and VLA-1. The HIV-infect ed individuals were subdivided into 'lung symptomatic' or 'lung asympt omatic' patients, depending on the presence or absence of secondary lu ng diseases besides HIV. All HIV-infected individuals demonstrated a d ecreased number of CD4(+) lymphocytes in blood; however, normal number s of these cells were found in BAL. The activation state of CD4(+) and CD8(+) 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 increase d 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 s ymptom-free subgroup. These results suggest that microorganisms other than HIV may promote viral replication via antigen-driven accumulation and activation of CD4(+) 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.