Role of adenoviruses in obesity

  title={Role of adenoviruses in obesity},
  author={Jameson D. Voss and Richard L. Atkinson and Nikhil V. Dhurandhar},
  journal={Reviews in Medical Virology},
  pages={379 - 387}
Five human adenovirus subtypes, Ad5, Ad9, Ad31, Ad36, and Ad37, and a non‐human adenovirus, SMAM1, are linked to increased adiposity in vitro or in vivo. Experimental infection with Ad5, Ad36, and Ad37 produced excess adiposity or weight gain in animals. Ad9 and Ad31 increase fat storage in tissue culture but are not associated with animal or human obesity. Ad36 is the most extensively studied adipogenic adenovirus and is correlated with some measure of overweight/obesity in humans from… 

Infectobesity: the evaluation of adenovirus-36 infection and obesity

A large-scale study incorporating various ethnicities and age groups is required to investigate the worldwide epidemic of obesity and its links with viruses.

Using rats as a research model to investigate the effect of human adenovirus 36 on weight gain

Rats can be used as a good animal model for further investigations about Ad-36-induced obesity, provided not to rely merely on weight measurements, and longer follow-up duration is needed to develop a significant weight gain in the infected rats.

Adenovirus 36 improves glycemic control and markers of Alzheimer's disease pathogenesis.

Adenovirus 5 produces obesity and adverse metabolic, morphological, and functional changes in the long term in animals fed a balanced diet or a high-fat diet: a study on hamsters

The chronic effects of Ad-5 infection on golden (Syrian) hamsters fed either a balanced diet (BD) or a high-fat diet (HFD) and an obesity paradox is presented: at the end of the study, the animals that had the most morphological and functional changes had the lowest body weight.

Adipocyte commitment of 3T3-L1 cells is required to support human adenovirus 36 productive replication concurrent with altered lipid and glucose metabolism

The results show that only adipocyte-committed 3T3-L1 cells are permissive for the expression of early and late viral mRNAs, as well as viral DNA replication and progeny production, supporting productive HAdV-D36 viral replication, indicating that a greater effect on adipogenesis occurs in adipocytes that support productive viral replication.

Viral Infections and Interferons in the Development of Obesity

Evidence is examined indicating that gut microbiota uphold intrinsic IFN signaling, which is extensively involved in the regulation of lipid metabolism, and the prolonged IFN responses during persistent viral infections and obesogenesis comprise reciprocal causality between virus susceptibility and obesity.

Viral Infections and Obesity

The evidence for a role in the genesis of obesity for viral agents in five broad categories is addressed: adenoviridae, herpesviridae, phages, transmissible spongiform encephalopathies (slow virus), and other encephalitides and hepatitides.

Immunometabolic Links Underlying the Infectobesity with Persistent Viral Infections

  • Yongming Sang
  • Biology, Medicine
    Journal of Immunological Sciences
  • 2019
From an immunological view, some infections, particularly chronic viral infections as focused here, are associated and even form a reciprocal causality with obesity through their pathogenic intervention with host immune and metabolic systems at various stages of obesity development.

Mouse Adenovirus Type 1 Persistence Exacerbates Inflammation Induced by Allogeneic Bone Marrow Transplantation

The results suggest that MAV-1 persists in multiple sites without detectable evidence of ongoing replication, and indicate that adenovirus persistence alters host responses to an unrelated challenge, even in the absence of detectable reactivation.



Genomic stability of adipogenic human adenovirus 36

There were no mutations in the E4orf1 gene, the critical gene for producing obesity, and the very-low-variation rate of Ad36 should reduce concerns about genetic variability when developing Ad36 vaccines or developing assays for detecting Ad36 infection in populations.

Adipogenic potential of multiple human adenoviruses in vivo and in vitro in animals.

Ad-37 is another human adenovirus that increases adiposity and reduces serum triglycerides in an animal model, however, the response of serum cholesterol is opposite that of Ad-36.

Obesity-independent Association of Human Adenovirus Ad37 Seropositivity With Nonalcoholic Fatty Liver Disease

Because fatty liver improves even without weight loss by a “healthy” diet, and not only by lower food caloric intake, Ad37+ may be an adjunctive hallmark of an unfavorable clinical-metabolic profile, if not a causative factor of NAFLD.

Human obesity relationship with Ad36 adenovirus and insulin resistance

The results do not support that any Ad36 adipogenic adenovirus effect is operating in human obesity through an insulin-resistance-related mechanism, and a significant association of Ad36 seropositivity with obesity and with essential hypertension in human beings is suggested.

Adipogenic human adenovirus-36 reduces leptin expression and secretion and increases glucose uptake by fat cells

The in vitro and ex vivo studies show that Ad-36 modulates adipocyte differentiation, leptin production and glucose metabolism, and whether such a modulation contributes to enhanced adipogenesis and consequent adiposity in Ad- 36 infected animals or humans needs to be determined.

Human adenovirus-36 is associated with increased body weight and paradoxical reduction of serum lipids

Ad-36 is associated with increased body weight and lower serum lipids in humans and Prospective studies are indicated to determine if Ad-36 plays a role in the etiology of human obesity.

Human adenovirus Ad-36 promotes weight gain in male rhesus and marmoset monkeys.

It is illustrated that the adiposity-promoting effect of Ad-36 occurs in two nonhuman primate species and demonstrates the usefulness of nonhuman primates for further evaluation ofAd-36-induced adiposity.

Adenovirus 36 as an obesity agent maintains the obesity state by increasing MCP-1 and inducing inflammation.

  • Ha-Na NaJ. Nam
  • Biology, Medicine
    The Journal of infectious diseases
  • 2012
The proposition that virus-induced inflammation is the cellular mechanism underlying Ad36-induced obesity is supported and it is suggested that MCP-1 plays a critical role in Ad36 -induced obesity and that M CP-1 may be a therapeutic target in preventing virus- induced obesity.

Insulin sparing action of adenovirus 36 and its E4orf1 protein.

  • N. Dhurandhar
  • Biology, Medicine
    Journal of diabetes and its complications
  • 2013

Human adenovirus Ad-36 induces adipogenesis via its E4 orf-1 gene

Ad-36 E4 orf-1 is a novel inducer of rodent and human adipocyte differentiation process and spanned the entire adipogenic cascade ranging from the upregulation of cAMP, phosphatidylinositol 3-kinase and p38 signaling pathways, and downregulation of Wnt10b expression.