PMID- 19502044
OWN - NLM
STAT- MEDLINE
DCOM- 20100830
LR  - 20211020
IS  - 1532-3064 (Electronic)
IS  - 0954-6111 (Print)
IS  - 0954-6111 (Linking)
VI  - 103
IP  - 11
DP  - 2009 Nov
TI  - Role of genetic susceptibility to latent adenoviral infection and decreased lung 
      function.
PG  - 1672-80
LID - 10.1016/j.rmed.2009.05.008 [doi]
AB  - BACKGROUND: Latent adenoviral infection may amplify cigarette smoke-induced lung 
      inflammation and therefore play an important role in the development of chronic 
      obstructive pulmonary disease (COPD). Adenoviruses can evade the human immune 
      response via their 19-kDa protein (19K) which delays the expression of class I 
      human leukocyte antigen (HLA) proteins. The 19K protein shows higher affinity to 
      HLA-B7 and A2 compared with HLA-A1 and A3. The receptor for adenovirus (CXADR) 
      and integrin beta(5) (ITGB5) are host factors which might affect adenovirus 
      infection. Therefore, we investigated the contribution of HLA, CXADR, and ITGB5 
      genetic variants to the presence of the E1A gene and to level of lung function. 
      METHODS: Study subjects were assayed for HLA-B7, A1, A2 and A3 by PCR-based 
      assays using allele-specific primers. Polymorphisms of the CXADR and ITGB5 genes 
      were genotyped by PCR-based restriction fragment length polymorphism assays. 
      Detection of adenoviral E1A gene was performed by a real-time PCR TaqMan assay. 
      RESULTS: E1A positive individuals had a lower FEV(1) compared with E1A negative 
      individuals. However, there was no significant difference in E1A positivity rate 
      between the high (HLA-B7 and A2) and low (HLA-A1 and A3) 19K affinity groups. 
      There was also no significant difference in FEV(1) level between each affinity 
      group. There was no significant difference in E1A positivity rate or lung 
      function among the CXADR and ITGB5 genotypes. CONCLUSIONS: Genetic variants in 
      HLA, CXADR and ITGB5 do not influence latent adenoviral infections and are not 
      associated with COPD.
FAU - Kasuga, Ikuma
AU  - Kasuga I
AD  - The James Hogg iCAPTURE Centre, University of British Columbia, St Paul's 
      Hospital, Vancouver, Canada.
FAU - Hogg, James C
AU  - Hogg JC
FAU - Pare, Peter D
AU  - Pare PD
FAU - Hayashi, Shizu
AU  - Hayashi S
FAU - Sedgwick, Edward G
AU  - Sedgwick EG
FAU - Ruan, Jian
AU  - Ruan J
FAU - Wallace, Alison M
AU  - Wallace AM
FAU - He, Jian-Qing
AU  - He JQ
FAU - Zhang, Xiaozhu
AU  - Zhang X
FAU - Sandford, Andrew J
AU  - Sandford AJ
LA  - eng
GR  - R01 HL066569/HL/NHLBI NIH HHS/United States
GR  - R01 HL066569-01/HL/NHLBI NIH HHS/United States
GR  - 1R01HL066569-01/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20090606
PL  - England
TA  - Respir Med
JT  - Respiratory medicine
JID - 8908438
RN  - 0 (CLMP protein, human)
RN  - 0 (Coxsackie and Adenovirus Receptor-Like Membrane Protein)
RN  - 0 (HLA Antigens)
RN  - 0 (Integrin beta Chains)
RN  - 0 (Receptors, Virus)
RN  - 0 (integrin beta5)
SB  - IM
MH  - Adenovirus Infections, Human/*genetics/immunology
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Coxsackie and Adenovirus Receptor-Like Membrane Protein
MH  - Female
MH  - Forced Expiratory Volume
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease/*genetics
MH  - Genotype
MH  - HLA Antigens/*genetics/immunology
MH  - Humans
MH  - Integrin beta Chains/*genetics
MH  - Male
MH  - Middle Aged
MH  - Pulmonary Disease, Chronic Obstructive/*genetics/immunology/physiopathology
MH  - Receptors, Virus/*genetics
MH  - Respiratory Function Tests
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Risk Factors
MH  - Smoking/adverse effects
MH  - Surveys and Questionnaires
PMC - PMC2757510
MID - NIHMS118818
COIS- CONFLICT OF INTEREST No author has any conflict of interests to declare.
EDAT- 2009/06/09 09:00
MHDA- 2010/08/31 06:00
PMCR- 2010/11/01
CRDT- 2009/06/09 09:00
PHST- 2009/03/05 00:00 [received]
PHST- 2009/05/08 00:00 [revised]
PHST- 2009/05/08 00:00 [accepted]
PHST- 2009/06/09 09:00 [entrez]
PHST- 2009/06/09 09:00 [pubmed]
PHST- 2010/08/31 06:00 [medline]
PHST- 2010/11/01 00:00 [pmc-release]
AID - S0954-6111(09)00161-9 [pii]
AID - 10.1016/j.rmed.2009.05.008 [doi]
PST - ppublish
SO  - Respir Med. 2009 Nov;103(11):1672-80. doi: 10.1016/j.rmed.2009.05.008. Epub 2009 
      Jun 6.