Adenovirus 36 obesity treatment is an emerging area of scientific interest, though no approved therapies currently exist. Adenovirus 36 (Ad-36) is a common human virus that laboratory studies suggest may influence fat cell development and weight gain. Whilst research has found associations between Ad-36 antibodies and higher body mass index, there is no established causal link, and Ad-36 testing is not part of routine NHS obesity care. Current UK guidance from NICE focuses on evidence-based lifestyle interventions, pharmacotherapy, and bariatric surgery. This article examines the Ad-36-obesity connection, available treatment options, and NHS obesity management pathways.

What Is Adenovirus 36 and Its Link to Obesity?

Adenovirus 36 (Ad-36) is a human adenovirus that has attracted scientific interest due to its potential association with obesity. Adenoviruses are common pathogens that typically cause respiratory infections, conjunctivitis, and gastroenteritis. However, laboratory studies suggest that Ad-36 may have unique metabolic effects that distinguish it from other adenovirus serotypes.

Research dating back to the 1990s has suggested that Ad-36 infection may contribute to weight gain and adiposity in both animal models and humans. Laboratory studies suggest that Ad-36 can infect adipocytes (fat cells) and increase their differentiation and lipid accumulation, possibly through viral proteins such as E4orf1. The virus appears to upregulate specific genes involved in fat cell development whilst simultaneously enhancing glucose uptake into cells. In animal experiments, chickens and rodents infected with Ad-36 showed increased body fat despite consuming similar amounts of food as uninfected controls.

Epidemiological studies in humans have found that individuals with antibodies to Ad-36 (indicating previous exposure) tend to have higher body mass index (BMI) values compared to those without such antibodies. Systematic reviews and meta-analyses have documented these associations, though with heterogeneity across studies and limitations in serology methods. However, it is crucial to emphasise that there is no official link establishing Ad-36 as a direct cause of obesity in humans. The relationship remains correlational rather than definitively causal.

Obesity is a multifactorial condition influenced by genetics, diet, physical activity, socioeconomic factors, and potentially infectious agents. Whilst Ad-36 may represent one contributing factor in susceptible individuals, it does not explain the majority of obesity cases. The concept of 'infectobesity'—obesity caused by infectious agents—remains an area of ongoing investigation rather than established medical fact.

Ad-36 testing is not part of routine NHS care and is not recommended for obesity assessment or management. Patients concerned about their weight should focus on evidence-based obesity management strategies as outlined in NICE guidance.

Current Evidence on Adenovirus 36 Obesity Treatment Options

Currently, there are no specific treatments targeting adenovirus 36 infection for obesity management approved by the MHRA (Medicines and Healthcare products Regulatory Agency) or recommended by UK clinical guidelines. A search of MHRA-licensed products confirms that no Ad-36-specific diagnostics, antivirals, or vaccines are authorised for clinical use. The evidence base for Ad-36-specific interventions remains limited and confined to preclinical research.

Several theoretical approaches have been explored in laboratory settings only:

• Antiviral medications: No antiviral drugs have been developed specifically to target Ad-36 or tested in clinical trials for obesity treatment. General antiviral agents used for other conditions have not been evaluated for this indication.

• Vaccination strategies: Experimental vaccines against Ad-36 have shown promise in preventing weight gain in animal models in preclinical studies, but no human vaccines exist or are currently in development for clinical use.

• Immunomodulatory approaches: Preclinical research has investigated whether enhancing immune responses might clear Ad-36 infection and reverse metabolic effects, but this remains entirely experimental.

The lack of validated diagnostic tests for active Ad-36 infection in routine clinical practice further complicates treatment development. Antibody testing can indicate previous exposure but does not confirm ongoing infection or its metabolic impact. Most individuals who test positive for Ad-36 antibodies are asymptomatic and may have been infected years previously. Ad-36 serology is not indicated to guide obesity treatment and is not used in NHS obesity management pathways.

Importantly, even if Ad-36 contributes to obesity in some individuals, standard evidence-based obesity treatments remain effective regardless of viral status. There is no evidence suggesting that people with Ad-36 antibodies respond differently to conventional weight management strategies. Therefore, current clinical practice focuses on established obesity interventions as outlined in NICE guidance (CG189, NG7) rather than viral-specific therapies. Patients should follow NHS obesity management pathways regardless of Ad-36 status.

NHS and NICE Guidance on Obesity Management

The National Institute for Health and Care Excellence (NICE) provides comprehensive guidance on obesity assessment and management through several key documents, including CG189 (Obesity: identification, assessment and management), NG7 (Preventing excess weight gain), and QS127 (Obesity: clinical assessment and management quality standard). These guidelines do not reference adenovirus 36 or other infectious causes, focusing instead on evidence-based interventions with proven efficacy.

NICE recommends a tiered approach to obesity management:

• Assessment: Calculate BMI and measure waist circumference. For most adults, obesity is defined as BMI ≥30 kg/m². For people of South Asian, Chinese, other Asian, Middle Eastern, Black African or African-Caribbean family origin, use lower BMI thresholds to trigger action: BMI ≥23 kg/m² indicates increased risk and BMI ≥27.5 kg/m² indicates high risk, warranting earlier intervention. Assess for comorbidities including type 2 diabetes, hypertension, dyslipidaemia, cardiovascular disease, and obstructive sleep apnoea.

• First-line interventions (Tier 1–2): Multicomponent lifestyle programmes incorporating dietary modification, increased physical activity, and behavioural strategies. These should be tailored to individual preferences and circumstances, with realistic goal-setting (initial target of 5–10% weight loss over 3–6 months). Tier 2 services typically provide structured group or individual programmes delivered in community settings.

• Specialist services (Tier 3): Multidisciplinary weight management services for people with complex obesity or significant comorbidities. Tier 3 services provide intensive lifestyle interventions, pharmacotherapy, and pre-bariatric surgery assessment. Referral criteria vary locally but typically include BMI ≥40 kg/m² or BMI ≥35 kg/m² with comorbidities.

• Pharmacological treatment: Consider as an adjunct to lifestyle interventions for adults with BMI ≥28 kg/m² with associated risk factors or BMI ≥30 kg/m². Options include orlistat, GLP-1 receptor agonists (liraglutide, semaglutide), and naltrexone/bupropion (availability may vary locally). Pharmacotherapy is typically initiated and monitored within specialist services (Tier 3) according to NICE technology appraisals.

• Bariatric surgery (Tier 4): Consider for people with BMI ≥40 kg/m² or BMI 35–40 kg/m² with significant comorbidities when non-surgical measures have been unsuccessful. For people with recent-onset type 2 diabetes, consider bariatric surgery at BMI 30–34.9 kg/m² if inadequate glycaemic control despite optimal medical management, and expedite assessment. Surgery should be undertaken only by multidisciplinary teams with expertise in bariatric care.

The NHS provides obesity services through primary care, community weight management programmes (Tier 2), and specialist tier 3 and tier 4 services. Patients concerned about their weight should contact their GP for assessment and appropriate referral to evidence-based programmes. Referral pathways from primary care to specialist services vary by local commissioning arrangements.

Lifestyle Interventions and Medical Treatments for Obesity

Regardless of potential viral contributions to obesity, lifestyle modification remains the cornerstone of effective weight management. Evidence-based interventions have demonstrated consistent benefits across diverse populations.

Dietary approaches should focus on creating a sustainable calorie deficit whilst ensuring nutritional adequacy. NICE CG189 recommends reducing total energy intake by 600 kcal/day for most adults. Effective strategies include:

• Reducing portion sizes and energy-dense foods (high in fat and sugar)

• Increasing consumption of fruits, vegetables, and whole grains

• Limiting sugar-sweetened beverages and alcohol

• Considering structured approaches such as the Mediterranean diet or low-carbohydrate diets, depending on individual preference and metabolic profile

Physical activity provides multiple benefits beyond calorie expenditure, including improved insulin sensitivity, cardiovascular health, and psychological wellbeing. The UK Chief Medical Officers' Physical Activity Guidelines recommend:

• At least 150 minutes of moderate-intensity aerobic activity weekly (or 75 minutes vigorous intensity)

• Muscle-strengthening activities on at least two days per week to preserve lean muscle mass during weight loss

• Reducing sedentary time throughout the day

Behavioural strategies enhance long-term adherence and include self-monitoring (food diaries, activity tracking), goal-setting, stimulus control, and cognitive restructuring to address emotional eating patterns.

Pharmacological treatments licensed in the UK include:

• Orlistat (Xenical 120 mg prescription; alli 60 mg over-the-counter): Inhibits pancreatic and gastric lipases, reducing dietary fat absorption by approximately 30%. Common adverse effects include gastrointestinal symptoms (steatorrhoea, faecal urgency, oily spotting), which can be minimised by reducing fat intake to <30% of total energy. Consider a multivitamin supplement taken at bedtime (at least 2 hours after orlistat) due to reduced absorption of fat-soluble vitamins (A, D, E, K). Review treatment at 12 weeks; discontinue if weight loss is less than 5% of initial body weight. Important interactions include ciclosporin (separate doses by at least 2 hours), warfarin (monitor INR), levothyroxine (separate doses by at least 4 hours), and antiepileptic drugs (monitor for seizure control). Contraindications include chronic malabsorption syndrome and cholestasis.

• GLP-1 receptor agonists: Semaglutide 2.4 mg subcutaneous injection once weekly (Wegovy) and liraglutide 3 mg subcutaneous injection once daily (Saxenda) enhance satiety and reduce appetite through central and peripheral mechanisms. These agents also improve glycaemic control in people with type 2 diabetes. NICE technology appraisals specify use within specialist weight management services for adults with BMI ≥35 kg/m² (or ≥32.5 kg/m² for some ethnic groups) and at least one weight-related comorbidity. Adverse effects include nausea, vomiting, diarrhoea, and constipation, typically diminishing with dose titration and continued use. Important cautions include risk of pancreatitis, gallbladder disease (cholelithiasis, cholecystitis), dehydration, and hypoglycaemia (if used with insulin or sulfonylureas). Contraindicated in pregnancy. Review at 6 months (semaglutide) or 12 weeks (liraglutide); discontinue if inadequate weight loss (<5% for liraglutide; <5% at 6 months for semaglutide). Continuation beyond initial period requires ongoing weight loss and clinical benefit.

• Naltrexone/bupropion (Mysimba): Combination product acting on central appetite regulation. Licensed in the UK but availability may be restricted by local formularies. Typically initiated within specialist services. Key contraindications include uncontrolled hypertension, seizure disorders, current or prior diagnosis of bulimia or anorexia nervosa, chronic opioid or opiate agonist use (including opioid dependence treatment), acute alcohol or benzodiazepine withdrawal, and pregnancy. Common adverse effects include nausea, constipation, headache, and dizziness. Monitor blood pressure regularly. Review at 16 weeks; discontinue if weight loss <5% of initial body weight.

Patients should seek medical advice before starting any weight loss medication and report concerning symptoms promptly, including severe abdominal pain, persistent vomiting, symptoms suggestive of pancreatitis (severe upper abdominal pain radiating to the back) or gallbladder disease (right upper quadrant pain, jaundice), or signs of dehydration. Suspected adverse drug reactions should be reported via the MHRA Yellow Card Scheme at yellowcard.mhra.gov.uk or using the Yellow Card app.

Future Research Directions in Viral Obesity Treatments

The concept of infectobesity, whilst intriguing, requires substantial further investigation before translating into clinical practice. Several research priorities have been identified by the scientific community, as outlined in contemporary reviews on infectobesity and the metabolic virome.

Establishing causality remains the primary challenge. Whilst associations between Ad-36 antibodies and obesity have been documented in systematic reviews and meta-analyses, correlation does not prove causation. Prospective longitudinal studies tracking individuals from the point of Ad-36 infection through subsequent weight changes would provide stronger evidence. Such studies must account for confounding variables including diet, physical activity, genetic predisposition, and socioeconomic factors.

Mechanistic research continues to explore how Ad-36 might influence metabolism at the molecular level. Key questions include:

• Which specific viral proteins (such as E4orf1) mediate adipogenic effects?

• How does the virus interact with host metabolic pathways and gene expression?

• Can viral effects be reversed after clearance of infection?

• Do individual genetic variations influence susceptibility to Ad-36-induced weight gain?

Diagnostic development would enable identification of individuals with active Ad-36 infection versus historical exposure. Current antibody tests cannot distinguish between these states, limiting their clinical utility.

Therapeutic interventions under theoretical consideration include antiviral drugs, vaccines, and immunotherapies. However, these remain in early preclinical stages with no human trials to date. Any future treatments would need to demonstrate safety and efficacy through rigorous clinical trials before regulatory approval by the MHRA.

Broader microbiome and virome research is examining how various microorganisms (bacteria, viruses, fungi) influence metabolism and obesity risk. Early-stage research suggests that the gut virome—the collection of viruses inhabiting the gastrointestinal tract—may play previously unrecognised roles in energy homeostasis, but clinical applications are not established.

It is important to emphasise that current obesity management should not await these future developments. Evidence-based lifestyle, pharmacological, and surgical interventions as outlined in NICE guidance (CG189, NG7) and NICE technology appraisals remain effective and should be implemented according to established NHS pathways. Patients concerned about obesity should focus on proven strategies available through their GP and NHS weight management services whilst the scientific community continues to explore novel mechanisms and potential treatments.

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