PMID- 30728828
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1664-8021 (Print)
IS  - 1664-8021 (Electronic)
IS  - 1664-8021 (Linking)
VI  - 9
DP  - 2018
TI  - Interaction of the Host and Viral Genome and Their Influence on HIV Disease.
PG  - 720
LID - 10.3389/fgene.2018.00720 [doi]
LID - 720
AB  - The course of Human Immunodeficiency Virus type 1 (HIV) infection is a dynamic 
      interplay in which both host and viral genetic variation, among other factors, 
      influence disease susceptibility and rate of progression. HIV set-point viral 
      load (spVL), a key indicator of HIV disease progression, has an estimated 30% of 
      variance attributable to common heritable effects and roughly 70% attributable to 
      environmental factors and/or additional non-genetic factors. Genome-wide 
      genotyping and sequencing studies have allowed for large-scale association 
      testing studying host and viral genetic variants associated with infection and 
      disease progression. Host genomics of HIV infection has been studied 
      predominantly in Caucasian populations consistently identifying human leukocyte 
      antigen (HLA) genes and C-C motif chemokine receptor 5 as key factors of HIV 
      susceptibility and progression. However, these studies don't fully assess all 
      classes of genetic variation (e.g., very rare polymorphisms, copy number variants 
      etc.) and do not inform on non-European ancestry groups. Additionally, viral 
      sequence variability has been demonstrated to influence disease progression 
      independently of host genetic variation. Viral sequence variation can be 
      attributed to the rapid evolution of the virus within the host due to the 
      selective pressure of the host immune response. As the host immune system 
      responds to the virus, e.g., through recognition of HIV antigens, the virus is 
      able to mitigate this response by evolving HLA-specific escape mutations. 
      Diversity of viral genotypes has also been correlated with moderate to strong 
      effects on CD4+ T cell decline and some studies showing weak to no correlation 
      with spVL. There is evidence to support these viral genetic factors being 
      heritable between individuals and the evolution of these factors having important 
      consequences in the genetic epidemiology of HIV infection on a population level. 
      This review will discuss the host-pathogen interaction of HIV infection, explore 
      the importance of host and viral genetics for a better understanding of 
      pathogenesis and identify opportunities for additional genetic studies.
FAU - Tough, Riley H
AU  - Tough RH
AD  - JC Wilt Infectious Diseases Research Centre, Public Health Agency of Canada, 
      Winnipeg, MB, Canada.
AD  - Department of Medical Microbiology and Infectious Diseases, University of 
      Manitoba, Winnipeg, MB, Canada.
FAU - McLaren, Paul J
AU  - McLaren PJ
AD  - JC Wilt Infectious Diseases Research Centre, Public Health Agency of Canada, 
      Winnipeg, MB, Canada.
AD  - Department of Medical Microbiology and Infectious Diseases, University of 
      Manitoba, Winnipeg, MB, Canada.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190123
PL  - Switzerland
TA  - Front Genet
JT  - Frontiers in genetics
JID - 101560621
PMC - PMC6351501
OTO - NOTNLM
OT  - HIV infection
OT  - genetic epidemiology
OT  - genetic variation
OT  - genome-wide studies
OT  - host-pathogen interaction
OT  - set point viral load
EDAT- 2019/02/08 06:00
MHDA- 2019/02/08 06:01
PMCR- 2019/01/23
CRDT- 2019/02/08 06:00
PHST- 2018/10/12 00:00 [received]
PHST- 2018/12/21 00:00 [accepted]
PHST- 2019/02/08 06:00 [entrez]
PHST- 2019/02/08 06:00 [pubmed]
PHST- 2019/02/08 06:01 [medline]
PHST- 2019/01/23 00:00 [pmc-release]
AID - 10.3389/fgene.2018.00720 [doi]
PST - epublish
SO  - Front Genet. 2019 Jan 23;9:720. doi: 10.3389/fgene.2018.00720. eCollection 2018.