Host-pathogen interactions in emerging and re-emerging infectious diseases: A genomic perspective of tuberculosis, malaria, human immunodeficiency virus infection, hepatitis B, and cholera

被引:49
作者
McNicholl, JM [1 ]
Downer, MV
Udhayakumar, V
Alper, CA
Swerdlow, DL
机构
[1] Ctr Dis Control, Natl Ctr Infect Dis, Div AIDS STD & TB Lab Res, Atlanta, GA 30333 USA
[2] Ctr Dis Control, Natl Ctr Infect Dis, Div Parasit Dis, Atlanta, GA 30333 USA
[3] Ctr Dis Control, Natl Ctr Infect Dis, Div Bacterial & Mycot Dis, Atlanta, GA 30333 USA
[4] Ctr Blood Res Inc, Boston, MA 02115 USA
关键词
gene; polymorphism; susceptibility; resistance; vaccines;
D O I
10.1146/annurev.publhealth.21.1.15
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
On exposure to a pathogen, a host may resist infection, become subclinically infected, or progress through several stages from mild to severe infection. Chronic sequelae may or may not occur. Host factors, particularly host genes, influence many of these stages. We have used a model of the continuum of pathogenesis of infectious diseases to consider the effect of host genes on five pathogens of significant public health burden: Mycobacterium tuberculosis, Plasmodium species, human immunodeficiency virus, hepatitis B virus, and Vibrio cholerae. The relationships between these infections and polymorphisms in human leukocyte antigen, cytokines, other immune response, or pathogen receptor genes are reviewed. We discuss gene-gene interactions and their effects in complex settings, such as coinfections with several pathogens. Priorities for prevention and control of these pathogens include vaccines and antimicrobial drugs. Research on how host genes can influence vaccine responses and the efficacy of drugs or other interventions, as well as further research into the relationship of host genes to infectious disease outcomes, may lead to new strategies for prevention and control.
引用
收藏
页码:15 / 46
页数:32
相关论文
共 149 条
[1]   Genetic epidemiology of infectious diseases in humans: Design of population-based studies [J].
Abel, L ;
Dessein, AJ .
EMERGING INFECTIOUS DISEASES, 1998, 4 (04) :593-603
[2]   α+-thalassemia protects children against disease caused by other infections as well as malaria [J].
Allen, SJ ;
O'Donnell, A ;
Alexander, NDE ;
Alpers, MP ;
Peto, TEA ;
Clegg, JB ;
Weatherall, DJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (26) :14736-14741
[3]   PROTECTION AFFORDED BY SICKLE-CELL TRAIT AGAINST SUBTERTIAN MALARIAL INFECTION [J].
ALLISON, AC .
BRITISH MEDICAL JOURNAL, 1954, 1 (4857) :290-294
[4]   GENETIC PREDICTION OF NONRESPONSE TO HEPATITIS-B VACCINE [J].
ALPER, CA ;
KRUSKALL, MS ;
MARCUSBAGLEY, D ;
CRAVEN, DE ;
KATZ, AJ ;
BRINK, SJ ;
DIENSTAG, JL ;
AWDEH, Z ;
YUNIS, EJ .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 321 (11) :708-712
[5]   Impairment of mycobacterial immunity in human interleukin-12 receptor deficiency [J].
Altare, F ;
Durandy, A ;
Lammas, D ;
Emile, JF ;
Lamhamedi, S ;
Le Deist, F ;
Drysdale, P ;
Jouanguy, E ;
Döffinger, R ;
Bernaudin, F ;
Jeppsson, O ;
Gollob, JA ;
Meinl, E ;
Segal, AW ;
Fischer, A ;
Kumararatne, D ;
Casanova, JL .
SCIENCE, 1998, 280 (5368) :1432-1435
[6]  
[Anonymous], 1970, Bull World Health Organ, V43, P143
[7]  
[Anonymous], TRANSL ADV HUM GEN P
[8]   CCR2-64I allele and genotype association with delayed AIDS progression in African women [J].
Anzala, AO ;
Ball, TB ;
Rostron, T ;
O'Brien, SJ ;
Plummer, FA ;
Rowland-Jones, SL .
LANCET, 1998, 351 (9116) :1632-1633
[9]   Blocking chemokine receptors [J].
Baggiolini, M ;
Moser, B .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 186 (08) :1189-1191
[10]   ABO BLOOD-GROUPS AND CHOLERA [J].
BARUA, D ;
PAGUIO, AS .
ANNALS OF HUMAN BIOLOGY, 1977, 4 (05) :489-492