Adenovirus-36 prevalence paradox in development

Abstract

For decades, adenovirus-36 (AD-36) and infectobesity are part f an ongoing discussion within obesity research based on intrigung results described first in 1992 in animals by Dhurandhar et al.1 nd in 2005 in humans by Atkinson et al.2 Recently, this topic is ntroduced also in clinical virology by Esposito et al.3 Within this linical virological view, the authors indicate that available data including molecular results in animals and serological results n USA, Korea and Italy with AD-seroprevalences up to 30% and igher – do not completely solve the problem of the possible relaionship between AD-36 infection and obesity in humans.3 For erological results, as in the previous literature the authors indicate hat AD-36 is distinct from all other human adenoviruses in terms f neutralization and hemagglutination inhibition, and does not ross-react with other viruses.3 Besides molecular results in anials, also limited results in humans are available although maybe n a paradoxal way. Therefore we want to comment on the indicated pecificity of AD-36 serology and on a non-neglectable absence or on-detection of AD-36 in most adenoviral studies in humans. Few positive reports for AD-36 culture and/or PCR are available ince the isolation of the original AD-36 strain in 1978.4 In 2008, asarica and coworkers including Dhurandhar, described natural D-36 infection in 9 obese, normoglycemic Native American Pima ndians by PCR on subcutaneous abdominal adipose tissue.5 In 010, Salehian and coworkers including Atkinson, described the etection of AD-36 DNA in a patient with unusual visceral obesity.6 emarkable, as a control, samples of adipose tissue obtained by eedle fat biopsy from 12 obese persons without abnormal adiose tissue deposits were positive also. According to the authors, he prevalence of AD-36 infection identified by PCR was similar to hat identified by serum neutralization in obese adults in the United tates.6