PMID- 11778647
OWN - NLM
STAT- MEDLINE
DCOM- 20020423
LR  - 20180821
IS  - 1076-1551 (Print)
IS  - 1528-3658 (Electronic)
IS  - 1076-1551 (Linking)
VI  - 7
IP  - 9
DP  - 2001 Sep
TI  - Genetic determinants of pediatric HIV-1 infection: vertical transmission and 
      disease progression among children.
PG  - 583-9
AB  - It is very likely that perinatal human immunodeficiency virus type 1 (HIV-1) 
      infection is influenced by a combination of virologic and host factors. A greater 
      understanding of the role played by various risk factors for HIV-1 infection is 
      crucial for the design of new preventive and therapeutic strategies. In recent 
      years, a number of studies have suggested that host genetic factors are important 
      determinants of both the susceptibility to perinatal HIV-1 infection and the 
      subsequent pathogenesis of acquired immunodeficiency syndrome (AIDS). Control of 
      HIV-1 infection involves the processing of specific viral peptides and their 
      presentation to cells of the immune system by highly polymorphic human leukocyte 
      antigen (HLA) alleles. The contribution of multiple HLA class I and II alleles in 
      modulating pediatric HIV/AIDS outcomes has now been confirmed by several 
      independent groups. Penetration of HIV-1 into cells is mediated by interaction 
      between CD4 and chemokine receptors that serve as entry coreceptors. Genetic 
      polymorphisms in chemokine ligand and chemokine receptor genes have recently been 
      associated both with mother-to-child HIV-1 transmission and disease progression 
      in children. These observations suggest a key role for genetic factors in 
      pediatric HIV-1 infection. This article describes the current state of knowledge 
      regarding host genetic influences on pediatric HIV-1 infection and discusses the 
      role of these genes in HIV/AIDS pathogenesis.
FAU - Matt, C
AU  - Matt C
AD  - Laboratoire d'immunogenetique, Centre de Recherche du Centre Hospitalier de 
      l'Universite de Montreal, Quebec, Canada.
FAU - Roger, M
AU  - Roger M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Mol Med
JT  - Molecular medicine (Cambridge, Mass.)
JID - 9501023
RN  - 0 (HLA Antigens)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Receptors, HIV)
SB  - IM
MH  - Child
MH  - *Disease Progression
MH  - Female
MH  - HIV Infections/*genetics/immunology/transmission
MH  - *HIV-1/immunology/physiology
MH  - HLA Antigens/genetics/immunology
MH  - Humans
MH  - Infant
MH  - *Infectious Disease Transmission, Vertical
MH  - Polymorphism, Genetic
MH  - Receptors, Chemokine/genetics/metabolism
MH  - Receptors, HIV/genetics/metabolism
PMC - PMC1950069
EDAT- 2002/01/10 10:00
MHDA- 2002/04/24 10:01
PMCR- 2001/09/01
CRDT- 2002/01/10 10:00
PHST- 2002/01/10 10:00 [pubmed]
PHST- 2002/04/24 10:01 [medline]
PHST- 2002/01/10 10:00 [entrez]
PHST- 2001/09/01 00:00 [pmc-release]
PST - ppublish
SO  - Mol Med. 2001 Sep;7(9):583-9.