PMID- 17276368
OWN - NLM
STAT- MEDLINE
DCOM- 20070821
LR  - 20070205
IS  - 1386-6532 (Print)
IS  - 1386-6532 (Linking)
VI  - 37 Suppl 1
DP  - 2006 Dec
TI  - HHV-6 and the immune system: mechanisms of immunomodulation and viral escape.
PG  - S4-10
AB  - Clinical and experimental evidence indicates that human herpesvirus 6 (HHV-6) can 
      interfere with the function of the host immune system through a variety of 
      mechanisms. Both HHV-6A and B can infect, either productively or nonproductively, 
      several types of immune cells. The primary target for HHV-6 replication, both in 
      vitro and in vivo, is the CD4+ T lymphocyte, a pivotal cell in the generation of 
      humoral and cell-mediated adaptive immune responses. HHV-6A, but not B, also 
      replicates in various cytotoxic effector cells, such as CD8+ T cells, gammadelta 
      T cells and natural killer cells. In professional antigen-presenting cells like 
      macrophages and dendritic cells, HHV-6 infection is typically nonproductive; yet, 
      it induces dramatic functional abnormalities, including a selective suppression 
      of IL-12, a critical cytokine in the generation of Th1-polarized antiviral immune 
      responses. This and other immunomodulatory effects seem to be mediated by the 
      engagement of the primary HHV-6 receptor, CD46. Moreover, HHV-6 infection results 
      in a generalized loss of CD46 expression in lymphoid tissue, which may lead to an 
      aberrant activation of autologous complement. Additional mechanisms of 
      immunomodulation by HHV-6 include alterations in cell surface receptor expression 
      and cytokine/chemokine production. HHV-6 can also modulate influence responses 
      through the expression of virally-encoded homologs of chemokines and chemokine 
      receptors. By modulating specific antiviral immune responses, HHV-6 can 
      facilitate its own spread and persistence in vivo, as well as enhance the 
      pathogenic effects of other agents, such as human immunodeficiency virus.
FAU - Lusso, Paolo
AU  - Lusso P
AD  - Unit of Human Virology, Department of Biological and Technical Research (DIBIT), 
      San Rafaele Scientific Institute, Milano, Italy. paolo.lusso@hsr.it
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - J Clin Virol
JT  - Journal of clinical virology : the official publication of the Pan American 
      Society for Clinical Virology
JID - 9815671
RN  - 0 (Cytokines)
RN  - 9007-36-7 (Complement System Proteins)
SB  - IM
MH  - Acquired Immunodeficiency Syndrome/virology
MH  - CD4-Positive T-Lymphocytes/immunology/virology
MH  - Complement System Proteins/immunology
MH  - Cytokines/*biosynthesis
MH  - Disease Progression
MH  - HIV-1/pathogenicity
MH  - Herpesvirus 6, Human/immunology/pathogenicity
MH  - Humans
MH  - Lymphocyte Subsets/*virology
MH  - Roseolovirus Infections/*immunology/*virology
MH  - T-Lymphocytes/*virology
RF  - 67
EDAT- 2007/02/06 09:00
MHDA- 2007/08/22 09:00
CRDT- 2007/02/06 09:00
PHST- 2007/02/06 09:00 [pubmed]
PHST- 2007/08/22 09:00 [medline]
PHST- 2007/02/06 09:00 [entrez]
AID - S1386-6532(06)70004-X [pii]
AID - 10.1016/S1386-6532(06)70004-X [doi]
PST - ppublish
SO  - J Clin Virol. 2006 Dec;37 Suppl 1:S4-10. doi: 10.1016/S1386-6532(06)70004-X.