A comparison of viral fitness and virulence between emergent adenovirus 14p1 and prototype adenovirus 14p strains

被引:18
作者
Anderson, Benjamin D. [1 ]
Barr, Kelli L.
Heil, Gary L.
Friary, John A.
Gray, Gregory C.
机构
[1] Univ Florida, Dept Environm & Global Hlth, Coll Publ Hlth & Hlth Profess, Gainesville, FL 32610 USA
关键词
Adenoviruses; Virology; Viral diseases; Virulence; NEWCASTLE-DISEASE VIRUS; RESPIRATORY-DISEASE; OUTBREAK; PNEUMONIA; ILLNESS; THREAT; ALASKA; PCR;
D O I
10.1016/j.jcv.2012.03.006
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
Background: Epidemiological studies from the last decade have suggested that the morbidity and mortality associated with a newly emergent strain of human adenovirus (HAdV-14p1) is greater than other, more prevalent, adenovirus strains. Recent molecular analysis identified very minor genetic differences in HAdV-14p1 compared to prototype HAdV-14p. No studies have evaluated how these differences may affect virulence. Objective: To compare HAdV-14p1 and HAdV-14p strains for competitive fitness and virulence. Study design: We performed in vitro and molecular assays to evaluate growth kinetics, cellular infectivity, cytotoxicity, and plaque morphology of the two strains. Results: Growth kinetic data showed no viral replication at 30 degrees C and minimal differences at 37 degrees C for both strains. Cellular infectivity data showed propagation capabilities for both strains in a diverse array of cell lines, with human lung and kidney cells having the highest propagation potential. Cytotoxicity data indicated cellular distress differences induced by both strains of virus in the first 12 h, but similar distress levels between 12 and 48 h. Plaque morphology assays showed some differences in average plaque diameter. Conclusions: These data suggest that the increase in morbidity and mortality observed in recent HAdV-14p1 infections is not due to viral growth or cellular infectivity differences from the prototypic HAdV-14 strain. While there were some statistically important differences detected between strains in cytotoxicity and plaque morphology assays, it seems more likely that other factors, such as environmental stressors, co-infections, or individual host response are likely contributing to the increase in morbidity. (C) 2012 Elsevier B. V. All rights reserved.
引用
收藏
页码:265 / 268
页数:4
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