PMID- 10090406
OWN - NLM
STAT- MEDLINE
DCOM- 19990525
LR  - 20061115
IS  - 1079-9907 (Print)
IS  - 1079-9907 (Linking)
VI  - 19
IP  - 2
DP  - 1999 Feb
TI  - Role of interleukin-8 and transforming growth factor-beta1 in enhancement of 
      human cytomegalovirus replication by human T cell leukemia-lymphoma virus type I 
      in macrophages coinfected with both viruses.
PG  - 209-17
AB  - Human cytomegalovirus (HCMV) is one of the most frequent opportunistic agents 
      causing severe illness in chronic human T cell leukemia-lymphoma virus type I 
      (HTLV-I) infection. Our previous studies have shown that coinfection of 
      macrophages with HCMV and HTLV-I significantly enhances HCMV replication, 
      resulting in release of infectious HCMV from dually infected cells. We found that 
      double infection of macrophages with HCMV and HTLV-I induced a rapid production 
      of substantial amounts of interleukin-8 (IL-8) and transforming growth 
      factor-beta1 (TGF-beta1). Results of transfection studies demonstrated that the 
      tax gene product of HTLV-I was able to induce secretion of IL-8 and TGF-beta1. In 
      addition to its cytokine-inducing effect, the Tax protein could interact with 
      HCMV synergistically to result in production of much higher levels of IL-8 and 
      TGF-beta1 than expected on the basis of their separate activities. Treatment of 
      dually infected macrophage cultures with neutralizing antibodies to IL-8 and 
      TGF-beta1 led to a nearly 1000-fold decrease in release of infectious HCMV from 
      coinfected cells. Similar results were obtained when anti-IL-8 and anti-TGF-beta1 
      treatments were combined in macrophage cultures transfected with the tax gene 
      before HCMV infection. Our results suggest that the stimulatory effect of HTLV-I 
      Tax protein on HCMV replication in coinfected macrophages is largely mediated by 
      high levels of IL-8 and TGF-beta1 production.
FAU - Szabo, J
AU  - Szabo J
AD  - Institute of Microbiology, University Medical School, Debrecen, Hungary.
FAU - Bacsi, A
AU  - Bacsi A
FAU - Beck, Z
AU  - Beck Z
FAU - Kiss, J
AU  - Kiss J
FAU - Andirko, I
AU  - Andirko I
FAU - Toth, F D
AU  - Toth FD
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Interferon Cytokine Res
JT  - Journal of interferon & cytokine research : the official journal of the 
      International Society for Interferon and Cytokine Research
JID - 9507088
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Gene Products, tax)
RN  - 0 (Interleukin-8)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Antibodies, Monoclonal
MH  - Cell Line
MH  - Cytomegalovirus Infections/metabolism/*physiopathology
MH  - Gene Products, tax/immunology
MH  - HTLV-I Infections/metabolism/*physiopathology
MH  - Humans
MH  - Interleukin-8/biosynthesis/*physiology
MH  - Macrophages/*physiology
MH  - Transforming Growth Factor beta/biosynthesis/*physiology
MH  - *Virus Replication
EDAT- 1999/03/25 00:00
MHDA- 1999/03/25 00:01
CRDT- 1999/03/25 00:00
PHST- 1999/03/25 00:00 [pubmed]
PHST- 1999/03/25 00:01 [medline]
PHST- 1999/03/25 00:00 [entrez]
AID - 10.1089/107999099314351 [doi]
PST - ppublish
SO  - J Interferon Cytokine Res. 1999 Feb;19(2):209-17. doi: 10.1089/107999099314351.