PMID- 11106932
OWN - NLM
STAT- MEDLINE
DCOM- 20001222
LR  - 20240414
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 101
IP  - 3
DP  - 2000 Nov
TI  - Nitric oxide and virus infection.
PG  - 300-8
AB  - Nitric oxide (NO) has complex and diverse functions in physiological and 
      pathophysiological phenomena. The mechanisms of many events induced by NO are now 
      well defined, so that a fundamental understanding of NO biology is almost 
      established. Accumulated evidence suggests that NO and oxygen radicals such as 
      superoxide are key molecules in the pathogenesis of various infectious diseases. 
      NO biosynthesis, particularly through expression of an inducible NO synthase 
      (iNOS), occurs in a variety of microbial infections. Although antimicrobial 
      activity of NO is appreciated for bacteria and protozoa, NO has opposing effects 
      in virus infections such as influenza virus pneumonia and certain other 
      neurotropic virus infections. iNOS produces an excessive amount of NO for long 
      periods, which allows generation of a highly reactive nitrogen oxide species, 
      peroxynitrite, via a radical coupling reaction of NO with superoxide. Thus, 
      peroxynitrite causes oxidative tissue injury through potent oxidation and 
      nitration reactions of various biomolecules. NO also appears to affect a host's 
      immune response, with immunopathological consequences. For example, 
      overproduction of NO in virus infections in mice is reported to suppress type 1 
      helper T-cell-dependent immune responses, leading to type 2 helper T-cell-biased 
      immunological host responses. Thus, NO may be a host response modulator rather 
      than a simple antiviral agent. The unique biological properties of NO are further 
      illustrated by our recent data suggesting that viral mutation and evolution may 
      be accelerated by NO-induced oxidative stress. Here, we discuss these multiple 
      roles of NO in pathogenesis of virus infections as related to both non-specific 
      inflammatory responses and immunological host reactions modulated by NO during 
      infections in vivo.
FAU - Akaike, T
AU  - Akaike T
AD  - Department of Microbiology, Kumamoto University School of Medicine, Kumamoto, 
      Japan.
FAU - Maeda, H
AU  - Maeda H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Humans
MH  - Mutation
MH  - Nitric Oxide/immunology/*physiology
MH  - Oxidative Stress/physiology
MH  - Virus Diseases/etiology/immunology/*metabolism
MH  - Viruses/genetics
PMC - PMC2327086
EDAT- 2000/12/07 11:00
MHDA- 2001/02/28 10:01
PMCR- 2001/11/01
CRDT- 2000/12/07 11:00
PHST- 2000/12/07 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/12/07 11:00 [entrez]
PHST- 2001/11/01 00:00 [pmc-release]
AID - imm142 [pii]
AID - 10.1046/j.1365-2567.2000.00142.x [doi]
PST - ppublish
SO  - Immunology. 2000 Nov;101(3):300-8. doi: 10.1046/j.1365-2567.2000.00142.x.