Influence of Seropositivity against Adenovirus-36 on the Risk of Obesity and Insulin Resistance in the Child Population of Southern Chile.

Background: Previous infection with Adenovirus-36 (HAdv-D36) has been associated with adipogenesis and glycemic regulation in cell culture and animal models. In humans, HAdv-D36 antibodies correlate with increased obesity risk yet paradoxically enhance glycemic control across various demographics. This study assesses the association of HAdv-D36 seropositivity with obesity, lipid, and glycemic profiles among school-aged children. Methods: We evaluated 208 children aged 9-13, categorized by BMI z-scores into normal weight (-1 to +1), overweight (+1 to +2), and obese (>+3). Assessments included anthropometry, Tanner stage for pubertal development, and biochemical tests (relating to lipids, glucose, and insulin), alongside HAdv-D36 seropositivity checked via ELISA. Insulin resistance was gauged using Chilean pediatric criteria. Results: The cohort displayed a high prevalence of overweight/obesity. HAdv-D36 seropositivity was 5.4%, showing no correlation with nutritional status. Additionally, no link between HAdv-D36 seropositivity and lipid levels was observed. Notably, insulin levels and HOMA-RI were significantly lower in HAdv-D36 positive children (p < 0.001). No cases of insulin resistance were reported in the HAdv-D36 (+) group in our population. Conclusions: HAdv-D36 seropositivity appears to decrease insulin secretion and resistance, aligning with earlier findings. However, no association with obesity development was found in the child population of southern Chile.

Association between obesity and diabetes prevalence and COVID-19 mortality in Mexico: an ecological study.

INTRODUCTION: Mortality rates associated with COVID-19 vary widely between countries and, within countries, between regions. These differences might be explained by population susceptibility, environmental factors, transmission dynamics, containment strategies, and diagnostic approaches. We aimed to analyze if obesity and diabetes prevalence are associated with higher COVID-19 mortality rates in Mexico. METHODOLOGY: We analyzed the mortality rate for each of the 2,457 municipalities in Mexico, one of the countries with highest COVID-19 mortality rate, during the first seven months of the pandemic to identify factors associated with higher mortality, including demographic, health-related characteristics (prevalence of obesity, diabetes, and hypertension in adults older than 20 years old), and altitude. RESULTS: During the first seven months of the COVID-19 pandemic there were 85,666 deaths reported in Mexico, with a cumulative mortality rate of 67 per 100,000 population. The mean mortality rate for the 2,457 municipalities in Mexico was 33.9 per 100,000 population. At a municipal level, the prevalence of diabetes and obesity, as well as high human development index, and location at < 500 or > 2000 above sea level were associated with higher mortality rate. CONCLUSIONS: Elevated obesity and diabetes prevalence explain, in part, high COVID-19 mortality rates registered in certain municipalities in Mexico. These results suggest that a regionalized approach should be considered to successfully limit the impact of SARS-CoV-2.

Maternal and Neonatal Outcomes of SARS-CoV-2 Infection in a Cohort of Pregnant Women with Comorbid Disorders.

There are some reports and case series addressing Coronavirus Disease 2019 (COVID-19) infections during pregnancy in upper income countries, but there are few data on pregnant women with comorbid conditions in low and middle income Countries. This study evaluated the proportion and the maternal and neonatal outcomes associated with SARS-CoV-2 infection among pregnant women with comorbidities. Participants were recruited consecutively in order of admission to a maternity for pregnant women with comorbidities. Sociodemographic, clinical, and laboratory data were prospectively collected during hospitalization. Pregnant women were screened at entry: nasopharyngeal swabs were tested by RT-PCR; serum samples were tested for IgG antibodies against spike protein by ELISA. From April to June 2020, 115 eligible women were included in the study. The proportion of SARS-CoV-2 infection was 28.7%. The rate of obesity was 60.9%, vascular hypertension 40.0%, and HIV 21.7%. The most common clinical presentations were ageusia (21.2%), anosmia (18.2%), and fever (18.2%). Prematurity was higher among mothers who had a SARS-CoV-2 infection based on RT-PCR. There were two cases of fetal demise. We found a high proportion of COVID-19 among pregnant women with comorbidities. This underscores the importance of antenatal care during the pandemic to implement universal SARS-CoV-2 screening, precautionary measures, and the rollout of vaccination programs for pregnant women.

Adenovirus 36 prevalence and association with human obesity: a systematic review.

INTRODUCTION: Obesity has numerous etiologies and includes biological factors. Studies have demonstrated that the human adenovirus subtype 36 (Adv36) is an adipogenic agent and causes metabolic alterations. Study results on the prevalence of Adv36 and clinical effects in humans vary substantially. This was a systematic review to summarize the studies on the prevalence of Adv36 infection and its association with human obesity. METHODS: A systematic literature review was conducted using the preferred reporting items for systematic reviews and meta-analysis (PRISMA). Observational or experimental studies found in the Medline, Embase, LILACS, Science Direct and SciELO databases that presented results on the prevalence of Adv36 in humans were included. RESULTS: Thirty-seven studies were screened. A total of 10,300 adults aged 18-70 years and 4585 children and adolescents aged 3-18 years were assessed. The average prevalence of Adv36 among adults was 22.9%, ranging from 5.5% to 49.8%. Among children and adolescents, the average prevalence of Adv36 was 28.9%, ranging from 7.5% to 73.9%. There was a positive statistical relationship between Adv36 and weight gain, obesity, or metabolic changes in 31 studies. However, in four studies there was no association with obesity, and in one, no association was described. One of the studies showed an inverse correlation, i.e., Adv36 was a protective factor against obesity. CONCLUSION: Strong evidence suggested a positive association between viral infection and obesity. However, due to the multi-causality of obesity and heterogeneity of studies, diagnostic tests should be standardized and easily accessible by the population to estimate the overall prevalence of Adv36 infection and its association with obesity.

Adenovirus-36 as one of the causes of obesity: the review of the pathophysiology.

The dramatic increase of people affected by obesity worldwide seems to be influenced by external factors independent of eating habits, physical exercise, or genetic characteristics. There may be a number of such factors, but one hypothesis is that there is person-to-person transmission, causing an epidemic effect, as occurs with infectious diseases. In animal models, experimental infection with human adenovirus-36 (Adv36) causes obesity. Humans cannot be experimentally infected, but a number of studies found a correlation of positive serology for Adv36 with overweight/obesity in humans. In vitro studies have shown that Adv36 accelerates the differentiation and proliferation of preadipocytes into adipocytes and increases their lipid concentration. Another viral mechanism involved is the activation of a noninsulin-dependent process that increases glucose uptake, mainly in adipose tissue and muscle. The increased glucose, coupled with increased lipogenesis due to increased fatty acid synthase and the action of peroxisome proliferator-activated receptor gamma (PPAR-gamma) in stimulating adipocyte differentiation from adult stem cells enhances fat accumulation within the adipocytes. In studies conducted to date, the Adv36 E4 open reading frame 1 gene (E4orf1), which activates the glucose transporter protein isoform 4 (GLUT4) and glucose transporter protein isoform 1 (GLUT1) glucose transporters, appears to play a major role in the virus adipogenesis. The aim of this study was to review the pathophysiology of obesity and the role of Adv36.

Nutritional status, diet and viral respiratory infections: perspectives for severe acute respiratory syndrome coronavirus 2.

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was recognised by the WHO as a pandemic in 2020. Host preparation to combat the virus is an important strategy to avoid COVID-19 severity. Thus, the relationship between eating habits, nutritional status and their effects on the immune response and further implications in viral respiratory infections is an important topic discussed in this review. Malnutrition causes the most diverse alterations in the immune system, suppressing of the immune response and increasing the susceptibility to infections such as SARS-CoV-2. On the other hand, obesity induces low-grade chronic inflammation caused by excess adiposity, which increases angiotensin-converting enzyme 2. It decreases the immune response favouring SARS-CoV-2 virulence and promoting respiratory distress syndrome. The present review highlights the importance of food choices considering their inflammatory effects, consequently increasing the viral susceptibility observed in malnutrition and obesity. Healthy eating habits, micronutrients, bioactive compounds and probiotics are strategies for COVID-19 prevention. Therefore, a diversified and balanced diet can contribute to the improvement of the immune response to viral infections such as COVID-19.

Incidence of COVID-19 infection and prevalence of diabetes, obesity and hypertension according to altitude in Peruvian population.

To investigate the cumulative incidence and mortality of COVID-19 and the prevalence of comorbidities such as diabetes, obesity and hypertension in regions with different altitude levels ranging from sea level to high altitude. METHODOLOGY: Analytical study in which we correlated secondary data obtained from reports of the Ministry of Health and National Institute for Statistics and Informatic. The cumulative incidence and mortality of COVID-19 in 25 peruvian regions is reported, together with its relationnship with altitude levels during March-July 2020 using Pearsons correlation. We also aiming to assess the prevalence of diabetes, obesity and hypertension with altitude according to the ENDES 2018 data using Gamma statistics. RESULTS: COVID-19 maintained an inverse correlation with higher rates in the coastal regions and lower rates with increasing altitude in the cumulative incidence (Pearson = -0.8, p < 0.000) and mortality (Pearson = -0.77, p < 0.000), adjusted gender and age. The prevalence of diabetes and obesity showed the same inverse correlation trend with altitude (Gamma p < 0.000) but not hypertension (Gamma p = 0.13) CONCLUSIONS: The data in Peru it is suggested that physiological adaptation in a hypoxic environment at high altitude may protect persons from the severe impact of acute infection caused by SARS-CoV-2. The reduction in cumulative incidence and mortality rates with increasing altitude is the main finding. Possible mechanisms such as a decreased expression of angiotensin-converting enzyme 2 (ACE2) and a lower virulence because of a high altitude environment, may explain this epidemiological features. In addition, the lower prevalence of diabetes, obesity and hypertension may establish a protective epidemiology against these disease.

COVID-19, Obesity, and Undernutrition: A Major Challenge for Latin American Countries.

In March of 2020, the World Health Organization declared the SARS­Cov2 2019 (COVID­19) outbreak a global pandemic after documenting community scale transmission in every region, including Latin America. The risk factors associated with severity of disease include older age, diabetes, hypertension, cardiovascular and lung diseases, and immune suppression. Additional evidence strongly suggests that obesity is also a risk factor for severe forms of COVID­19 disease, while other types of malnutrition increase the risk of hospitalization from influenza­like diseases, regardless of the causative agent of the illness (1). Although detailed data are not yet available on the impact of under nutrition in the evolution of COVID­19, given the known inflammatory response caused by this condition, it is reasonable to expect a suboptimal immune response and higher risk of severity, as found with obesity (2).

The Association of Obesity, Type 2 Diabetes, and Hypertension with Severe Coronavirus Disease 2019 on Admission Among Mexican Patients.

OBJECTIVE: This study's aim was to explore the association of obesity, type 2 diabetes, and hypertension with severe coronavirus disease 2019 (COVID-19) on admission. METHODS: In the present study, a total of 23,593 patient samples were evaluated by a laboratory from the Mexican Institute of Epidemiological Diagnosis and Reference. Of these, 18,443 were negative for COVID-19, 3,844 were positive for COVID-19, and 1,306 were positive for other respiratory viruses. Severe types of respiratory disease were defined by the presence of pneumonia and other organ failure that requires intensive care. Multivariable logistic regression models were used to explore factors associated with severe COVID-19 on admission. RESULTS: Patients who tested positive for COVID-19 had a higher proportion of obesity (17.4%), diabetes (14.5%), and hypertension (18.9%) compared with those without a confirmed diagnosis. Compared with patients without obesity, those with obesity showed a 1.43-fold higher odds of developing severe COVID-19 on admission, whereas subjects with diabetes and hypertension showed a 1.87-fold and 1.77-fold higher odds of developing severe COVID-19 on admission, respectively. CONCLUSIONS: Obesity, diabetes, and hypertension were significantly associated with severe COVID-19 on admission and the association of obesity was stronger in patients < 50 years of age.

The association between body mass index and anal canal human papillomavirus prevalence and persistence: the HIM study.

Background: While receptive anal sex is an established risk factor for anal human papillomavirus (HPV) infection and squamous cell carcinoma of the anus (SCCA), people with anal HPV infection and SCCA commonly report no lifetime receptive anal sex suggesting other factors may also increase risk for anal HPV infection and persistence. Given potential associations between obesity and conditions that may cause perianal or anal canal lesions, we hypothesized that body mass index (BMI) was associated with HPV infection. Methods: Genotyping for 36 HPV types was conducted on anal canal specimens from men, ages 18-70, from Brazil, Mexico, and the USA. Eligibility included no history of genital warts or HIV. Evaluable specimens were collected from 328 men having sex with men (MSM) and 1348 men having sex with women (MSW) who reported no lifetime receptive anal sex. Prevalence of anal HPV infection and six-month persistence by BMI were estimated in addition to adjusted prevalence ratios for the association between BMI and HPV infection. Results: Among MSW, obese men had a higher prevalence of HPV-16 in the anal canal (3.1%), compared to normal weight men (1.3%) although 95% CI overlapped. Among MSM, prevalence of HPV decreased with increasing BMI. A similar pattern was observed for persistence. After adjustment for confounders, obese MSW had 2.4 times higher odds of HPV-16 compared to normal weight men. Conclusions: BMI may be positively associated with anal HPV (especially HPV-16) among MSW and negatively associated with anal HPV among MSM which supports continued universal HPV vaccination programs.

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.

Adenovirus 5 (Ad-5) infection is a common cause of acute respiratory infections and the main vector used in gene therapy. There are few studies on the relationship of Ad-5 to obesity. In the present study, we evaluated the chronic effects of Ad-5 infection on golden (Syrian) hamsters fed either a balanced diet (BD) or a high-fat diet (HFD). After a single inoculation with Ad-5 (1 × 107 pfu), the body weight of the animals was measured weekly. Medium-term (22 weeks) serum biochemical analyses and long-term (44 weeks) liver morphology, adiposity, and locomotive functionality (movement velocity) assessments were carried out. In the animals fed the BD, adenovirus infection produced hyperglycemia and hyperlipidemia. In the long term, it produced a 57% increase in epididymal pad fat and a 30% body weight gain compared with uninoculated animals. In addition, morphological changes related to non-alcoholic fatty liver disease (NAFLD) were observed. The animals fed the HFD had similar but more severe changes. In addition, the hamsters presented an obesity paradox: at the end of the study, the animals that had the most morphological and functional changes (significantly reduced movement velocity) had the lowest body weight. Despite the fact that an HFD appears to be a more harmful factor in the long term than adenovirus infection alone, infection could increase the severity of harmful effects in individuals with an HFD. Epidemiological studies are needed to evaluate the effect of adenovirus as a precursor of chronic liver and cardiovascular diseases, including the chronic effects of gene therapy.

Obesity Increases the Duration of Influenza A Virus Shedding in Adults.

Epidemiologic studies indicate that obesity increases the risk of severe complications and death from influenza virus infections, especially in elderly individuals. This work investigates the effect of obesity on the duration of viral shedding within household transmission studies in Managua, Nicaragua, over 3 seasons (2015-2017). Symptomatic obese adults were shown to shed influenza A virus 42% longer than nonobese adults (adjusted event time ratio [ETR], 1.42; 95% confidence interval [CI], 1.06-1.89); no association was observed with influenza B virus shedding duration. Even among paucisymptomatic and asymptomatic adults, obesity increased the influenza A shedding duration by 104% (adjusted ETR, 2.04; 95% CI, 1.35-3.09). These findings suggest that obesity may play an important role in influenza transmission.

[The potential contribution of adenovirus 36 to the development of obesity]. / Adenovirus 36 y su potencial contribución en el desarrollo de obesidad.

The evidence of the last 20 years shows a link between viral infections and obesity in animals and humans. There are five adenovirus which have been associated with development of obesity in animals. SMAM-1 virus was the first studied in humans associated with obesity. There is compelling evidence that Ad-36 virus could contribute to the development of obesity in humans and it is related with body mass index (BMI). This manuscript reviews the association between Ad-36 and the other four virus infections with obesity. An electronic search of articles in the databases PubMed and Scielo, with use of key words: obesity, infection, adipose tissue, Ad-36, 3T3-L1 was performed. The search was restricted "human" and "animals". The importance of the relationship between virus infections and obesity has increased over the past two decades. Ad-36 shows more compelling evidence in humans. There are reports involving this virus in the enhancement of adipogenesis, adipocyte differentiation, a lower secretion of leptin and an increased insulin sensitivity. Future work should focus in larger cohort studies to confirm this association, which explains the global obesity epidemic from a new perspective.

Adenovirus 36 y su potencial contribución en el desarrollo de obesidad / The potential contribution of adenovirus 36 to the development of obesity

The evidence of the last 20 years shows a link between viral infections and obesity in animals and humans. There are five adenovirus which have been associated with development of obesity in animals. SMAM-1 virus was the first studied in humans associated with obesity. There is compelling evidence that Ad-36 virus could contribute to the development of obesity in humans and it is related with body mass index (BMI). This manuscript reviews the association between Ad-36 and the other four virus infections with obesity. An electronic search of articles in the databases PubMed and Scielo, with use of key words: obesity, infection, adipose tissue, Ad-36, 3T3-L1 was performed. The search was restricted "human" and "animals". The importance of the relationship between virus infections and obesity has increased over the past two decades. Ad-36 shows more compelling evidence in humans. There are reports involving this virus in the enhancement of adipogenesis, adipocyte differentiation, a lower secretion of leptin and an increased insulin sensitivity. Future work should focus in larger cohort studies to confirm this association, which explains the global obesity epidemic from a new perspective.

Incidence of Diabetes Mellitus and Obesity and the Overlap of Comorbidities in HIV+ Hispanics Initiating Antiretroviral Therapy.

BACKGROUND: Cardiovascular disease (CVD) is a leading health threat for HIV+ patients on antiretroviral therapy (ART); cardiometabolic comorbidities are key predictors of risk. Data are limited on incidence of metabolic comorbidities in HIV+ individuals initiating ART in low and middle income countries (LMICs), particularly for Hispanics. We examined incidence of diabetes and obesity in a prospective cohort of those initiating ART in the Dominican Republic. METHODS: Participants ≥18 years, initiating ART <90 days prior to study enrollment, were examined for incidence of impaired fasting glucose (IFG), diabetes mellitus (DM), overweight, and obesity. Fasting plasma glucose (FPG) 100-125mg/dl defined IFG; FPG ≥126 mg/dl, diagnosis per medical record, or use of hypoglycemic medication defined DM. Overweight and obesity were BMI 25-30 and ≥30kg/m2, respectively. Dyslipidemia was total cholesterol ≥240mg/dl or use of lipid-lowering medication. Framingham risk equation was used to determine ten-year CVD risk at the end of observation. RESULTS: Of 153 initiating ART, 8 (6%) had DM and 23 (16%) had IFG at baseline, 6 developed DM (28/1000 person-years follow up [PYFU]) and 46 developed IFG (329/1000 PYFU). At baseline, 24 (18%) were obese and 36 (27%) were overweight, 15 became obese (69/1000 PYFU) and 22 became overweight (163/1000 PYFU). Median observation periods for the diabetes and obesity analyses were 23.5 months and 24.3 months, respectively. Increased CVD risk (≥10% 10-year Framingham risk score) was present for 13% of the cohort; 79% of the cohort had ≥1 cardiometabolic comorbidity, 48% had ≥2, and 13% had all three. CONCLUSIONS: In this Hispanic cohort in an LMIC, incidences of IFG/DM and overweight/obesity were similar to or higher than that found in high income countries, and cardiometabolic disorders affected three-quarters of those initiating ART. Care models incorporating cardiovascular risk reduction into HIV treatment programs are needed to prevent CVD-associated mortality in this vulnerable population.

Production of interferon α and ß, pro-inflammatory cytokines and the expression of suppressor of cytokine signaling (SOCS) in obese subjects infected with influenza A/H1N1.

BACKGROUND & AIMS: Obesity was recognized as an independent risk factor for morbidity and mortality during last influenza A/H1N1 pandemic. Mechanisms involved in the high mortality risk from obesity during influenza A virus include reduced type I interferon production and delayed pro-inflammatory response, which lead to a higher rate of morbidity and mortality in murine models. In this study, we evaluated the production of type I interferons, pro-inflammatory and anti-inflammatory cytokines in peripheral blood mononuclear cells (PBMCs) from obese and lean subjects with and without confirmed infection of influenza A/H1N1. The expression levels of the suppressor of cytokine signaling-1 (SOCS1), SOCS3 and nuclear factor-kB were also evaluated. METHODS: Cytokines were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and/or by ELISA in PBMCs stimulated with toll like receptor-3 (TLR-3) and TLR-7 ligands. The mRNA expression of SOCS1 and SOCS3 were evaluated by qRT-PCR. RESULTS: The obese volunteers infected with influenza A/H1N1 showed a diminished ability to produce type I interferon in response to TLR-3 ligand. Interestingly, the pro-inflammatory response was also affected in TLR-3 stimulated PBMCs. Obese influenza-free volunteers showed an increased basal expression of SOCS3, but not SOCS1. During influenza infection, SOCS1 and SOCS3 expression was higher in the lean infected volunteers in contrast to those who were obese infected. CONCLUSIONS: These data suggest that obesity is related to TLR-3 impairment and explain, at least in part, the inadequate immune response of obese individuals during infection with influenza A/H1N1 virus.

Infeccions as the etiology for obesity.

The role of infection on obesity development has been questioned since the early 1980's. Several studies on animals have shown that physiopathologic mechanisms through which infections can produce obesity do exist. At least eight types of obesity-inducing viruses have been identified in animals, especially poultry and mice. Studies on humans are far less convincing; however, two adenoviruses, Ad-36 and SMAM-1, have shown adipogenic properties. In vitro studies with 3T3-L1 cells stated the activation of the enzymatic pathway that leads to fatty tissue accumulation; in vivo studies have also detected higher levels of antibodies against such viruses on obese subjects. Although most known infections nowadays cause obesity through central nervous system lesions, the Ad-36 adenovirus infection affects fatty tissue directly, raising doubts regarding central role component in this case.

Infeccions as the etiology for obesity / Infecções na etiologia da obesidade

The role of infection on obesity development has been questioned since the early 1980's. Several studies on animals have shown that fisiopathologic mechanisms through which infections can produce obesity do exist. At least eight types of obesity-inducing viruses have been identified in animals, especially poultry and mice. Studies on humans are far less convincing; however, two adenoviruses, Ad-36 and SMAM-1, have shown adipogenic properties. In vitro studies with 3T3-L1 cells stated the activation of the enzymatic pathway that leads to fatty tissue accumulation; in vivo studies have also detected higher levels of antibodies against such viruses on obese subjects. Although most known infections nowadays cause obesity through central nervous system lesions, the Ad-36 adenovirus infection affects fatty tissue directly, raising doubts regarding central role component in this case.

Desde o início dos anos 1980, o papel das infecções tem sido debatido quanto à etiologia da obesidade. Diversos estudos em modelos animais têm demonstrado que mecanismos fisiopatológicos ativados pelas infecções podem induzir também à obesidade. Pelo menos oito tipos de obesidade induzidas por viroses foram caracterizadas em animais, especialmente em camundongos e galinhas. Estudos em humanos existem, mas são menos convincentes. No entanto, duas adenoviroses (Ad-36 e SMAN-1) apresentam características adipogênicas. Estudos in vitro com a linhagem celular 3T3-L1 demonstraram que ativações enzimáticas levam ao acúmulo de gordura celular. Estudos in vivo detectaram níveis elevados de anticorpos contra certas viroses especialmente em indivíduos obesos. A maioria das infecções potenciais causadoras de obesidade atua produzindo ativações ou lesões no sistema nervoso central. Por outro lado, a infecção por Ad-36 adenovírus afeta diretamente o tecido adiposo, expandindo dessa forma a etiologia viral da obesidade para mecanismos hipotalâmicos e periféricos.