PMID- 10563708
OWN - NLM
STAT- MEDLINE
DCOM- 19991123
LR  - 20190718
IS  - 0269-9370 (Print)
IS  - 0269-9370 (Linking)
VI  - 13
IP  - 16
DP  - 1999 Nov 12
TI  - Sustained plasma TNF-alpha and HIV-1 load despite resolution of other parameters 
      of immune activation during treatment of tuberculosis in Africans.
PG  - 2231-7
AB  - OBJECTIVE: To determine the impact of treatment of tuberculosis on plasma HIV-1 
      load in African subjects and to correlate viral load with response to treatment 
      and changes in immune activation. DESIGN: Clinical and microbiological responses, 
      immune activation parameters and plasma HIV-1 load were determined in 20 patients 
      with pulmonary tuberculosis and HIV-1 coinfection in Ghana, West Africa during 
      the first 3 months of anti-tuberculosis treatment. METHODS: Plasma HIV-1 load and 
      markers of immune activation were determined by commercially available assays. 
      Human leukocyte antigen (HLA)-DR incorporation into the HIV-1 envelope was 
      measured by using an immunomagnetic capture technique. RESULTS: Treatment of 
      tuberculosis resulted in significant improvements in weight and haemoglobin, a 
      high sputum smear conversion rate and marked reductions in mean plasma tumour 
      necrosis factor (TNF) receptor-1, interleukin-6 and C-reactive protein. 
      Furthermore, incorporation of host HLA-DR into the HIV-1 envelope decreased; this 
      also suggested a reduction in immune activation of the cells supporting viral 
      replication. However, of importance with regard to AIDS pathogenesis, neither 
      mean plasma TNF-alpha nor HIV-1 load decreased significantly. CONCLUSIONS: The 
      failure of HIV-1 plasma load to decline significantly during the initial months 
      of anti-tuberculosis treatment is associated with high, sustained systemic levels 
      of TNF-alpha. The dissociation between the sustained levels of plasma TNF-alpha 
      and the major reductions in other, diverse immune activation parameters may 
      represent dysregulation of cytokine production in these African patients.
FAU - Lawn, S D
AU  - Lawn SD
AD  - HIV and Retrovirology Branch, Centers for Disease Control and Prevention, Public 
      Health Service, U.S. Department of Health and Human Services, Atlanta, Georgia 
      30333, USA.
FAU - Shattock, R J
AU  - Shattock RJ
FAU - Acheampong, J W
AU  - Acheampong JW
FAU - Lal, R B
AU  - Lal RB
FAU - Folks, T M
AU  - Folks TM
FAU - Griffin, G E
AU  - Griffin GE
FAU - Butera, S T
AU  - Butera ST
LA  - eng
PT  - Journal Article
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (Antitubercular Agents)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - AIDS-Related Opportunistic Infections/*drug therapy/immunology/virology
MH  - Antitubercular Agents/*therapeutic use
MH  - Ghana
MH  - HIV-1/*isolation & purification
MH  - HLA-DR Antigens/immunology
MH  - Humans
MH  - Tuberculosis/complications/*drug therapy/immunology/virology
MH  - Tumor Necrosis Factor-alpha/*metabolism
MH  - Viral Load
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - 10.1097/00002030-199911120-00005 [doi]
PST - ppublish
SO  - AIDS. 1999 Nov 12;13(16):2231-7. doi: 10.1097/00002030-199911120-00005.