Calcutta School of Tropical Medicine

Tobacco use remains the leading preventable cause of morbidity and mortality worldwide, with current cessation therapies yielding suboptimal long-term abstinence. This systematic review evaluates the efficacy, tolerability, and neurobiological rationale of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dual GLP-1/glucose-dependent insulinotropic peptide (GIP) agonists in treating nicotine use disorder (NUD), with particular attention to smoking abstinence, craving reduction, weight gain mitigation, and mechanistic insights. Following PRISMA guidelines, a comprehensive search was conducted across PubMed, Embase, CENTRAL, PsycINFO, and Web of Science through April 2025. Eligible studies included randomized controlled trials (RCTs), observational cohorts, and preclinical rodent studies evaluating GLP-1 or GLP-1/GIP agonists in nicotine-related outcomes. Risk of bias was assessed using Cochrane RoB2, ROBINS-I, and SYRCLE tools. Narrative synthesis was conducted due to heterogeneity in study designs and outcome definitions. Twelve studies met inclusion criteria—eight human and four preclinical. Preclinical studies demonstrated consistent attenuation of nicotine-seeking behavior and mesolimbic dopaminergic signaling via GLP-1R agonism. Among human studies, exenatide showed the most robust efficacy in enhancing abstinence and reducing craving and weight gain. Dulaglutide did not improve abstinence, though it conferred metabolic benefits. Semaglutide showed indirect behavioral benefits in real-world observational data. Adverse events were predominantly mild gastrointestinal symptoms. GLP-1 RAs—particularly exenatide and semaglutide—exhibit promising neurobehavioral and metabolic effects in smoking cessation. Their dual mechanism may address key limitations of current pharmacotherapies. Larger, mechanistically enriched trials are warranted to validate efficacy and guide clinical translation for nicotine dependence and related substance use disorders.

This study aims to assess and compare the clinical presentations, laboratory parameters, radiological findings, and outcomes of adult patients infected with different dengue serotypes presenting to a tertiary care hospital in Kolkata, India, between July 2023 and April 2024Clinical presentations among different Dengue serotypesExamination & Radiological findings among different Dengue serotypes A prospective observational study was done on 140 dengue-positive patients aged >18 years. Other infections were excluded. Clinical features, laboratory parameters, imaging, and outcomes were analyzed across serotypes using R softwareLaboratory parameters among different Dengue serotypes and Inflammatory markers non severe vs severe DengueDengue severity and complications among different Dengue serotypes 140 cases (DENV2:48, DENV3:86, DENV4:6) mean age 34.4±12 years; 55.5% male : 44.5% female. 77 patients needed admission. Hypertension(36%) commonest comorbidity. All comorbidities found no severity difference among three groups. Common symptoms fever (99%), body ache (60%), myalgia (55%), headache (50%), and nausea (45%). Myalgia was more in DENV2 (p=0.009), arthralgia in DENV4 (p=0.04). Hematological, liver function tests, renal function tests were similar across 3 groups, except for higher triglycerides (198 mg/dL) and CRP (38.2 mg/dL) in DENV4; ferritin was lowest in DENV3 (482 ng/mL). On imaging gall bladder wall edema (18%) and splenomegaly (37%) were more seen in DENV2. No significant difference in dengue with warning signs across groups. Severe dengue(n=14) occurred in 14% DENV2 and 8% DENV3, none in DENV4. Secondary dengue (n=24) showed more warning signs than primary (87% vs 44%, p=0.001). Complications like plasma leakage, shock, and bleeding were comparable across serotypes without significant difference. One death occurred in a DENV2 patient due to DSS DENV2 and DENV3 were predominant serotypes. DENV2 showed more systemic symptoms and notable radiological changes. Elevated inflammatory markers were linked to severity. No major difference in severity or outcome were found across serotypes. Study limitation was no DENV1 and few DENV4 cases. Other studies showed various serotype severity, this study adds to existing knowledge showing minimal outcome variation by serotype. Larger multicentric studies and serotype surveillance are needed to clarify serotype-related risks as dengue virus changes its genes & epidemiology. In my knowledge this is latest study (2023-2024) from India comparing dengue serotypes difference All Authors: No reported disclosures

Introduction: Respiratory Syncytial Virus (RSV), a pathogenic virus, is one of the leading causes of acute respiratory tract infections, especially in infants, immunocompromised individuals and older adults. Prior to the Coronavirus Disease-2019 (COVID-19) pandemic, infections caused by this virus had a tendency to follow a predictable seasonal trend. The post-COVID picture of RSV has not been studied and there is a dearth of data, especially in the eastern part of the Indian subcontinent. Aim: To describe the distribution of RSV in the eastern part of India in the context of COVID-19. Materials and Methods: A retrospective study was carried out at a tertiary care hospital of West Bengal, namely Calcutta School of Tropical Medicine (Virology Unit) based on patient records of 954 Nasopharyngeal (NP) and Oropharyngeal (OP) swabs collected from indoor as well as outdoor patients between January 2021 and December 2024. The inclusion criterion was the presence of symptoms of lower respiratory tract infection, irrespective of age and gender. Following collection in appropriate Viral Transport Medium (VTM) containers and transport to the laboratory, maintaining cold chain, the samples were subjected to Ribonucleic Acid (RNA) extraction and real-time Reverse Transcriptase Polymerase Chain Reaction (rtRT-PCR). Results: Out of 954 samples tested, 244 (25.6%) were found to be positive for RSV. In 2021, 50 out of 51 (98.04%) RSV positive samples showed presence of RSV A, while in 2022 and 2023, 155 out of 157 (98.7%) and 28 out of 32 (87.5%) RSV positive samples showed presence of RSV B, respectively. Conclusion: The present study illustrates the behaviour of RSV in the context of the post-COVID scenario in eastern India, demonstrating the preponderance of RSV B since 2022 and showing its winter predominance in contrast to the summer predominance it displayed in the pre-COVID era.

The management of type 2 diabetes (T2D) has entered a new era with the advent of advanced incretin-based therapies. Therapeutic agents such as semaglutide and tirzepatide have demonstrated exceptional efficacy in improving glycemic control, inducing substantial weight loss, and reducing cardiometabolic risk, thereby redefining therapeutic expectations. Yet, dulaglutide retains a distinct role supported by its strong cardiovascular evidence base. The REWIND trial remains the only GLP-1 receptor agonist study to show a statistically significant reduction in major adverse cardiovascular events (MACE) in a predominantly primary prevention population, with durable benefit sustained over more than five years of follow-up. Comparative trials highlight that while tirzepatide and semaglutide deliver superior reductions in HbA1c and body weight, dulaglutide offers proven cardiovascular safety, favourable tolerability, and high persistence in real-world analyses. Its once-weekly, fixed-dose regimen requires no titration and is accessible across diverse healthcare systems in low- and middle-income countries, including those constrained by cost or resources. The SURPASS-CVOT established tirzepatide’s non-inferiority to dulaglutide for cardiovascular outcomes, reaffirming dulaglutide as an established comparator with robust outcome data. This narrative review collates evidence in this regard and argues that dulaglutide should be viewed not as superseded but as complementary offering a pragmatic balance of efficacy, safety, and accessibility that supports equitable cardiometabolic care worldwide.

The efficacy of cancer immunotherapy depends on the inherent immunogenicity of tumor cells, which is their ability to display recognizable antigens and stimulate effective immune responses. However, the immunogenic landscape of cancer is not static; it evolves through cancer immunoediting, a dynamic process that refines tumor antigenicity and sculpts immune evasion mechanisms. This immunogenic reprogramming often dictates therapeutic responsiveness, with many tumors acquiring immune resistance through defective antigen presentation, impaired interferon signaling, and the establishment of immunosuppressive microenvironments. Within this complex interplay, mutant p53 (mut-p53) has emerged as a pivotal regulator of tumor immunogenicity. Beyond its canonical oncogenic functions, gain-of-function (GOF) and other p53 mutants modulate antigen processing, repress immune-stimulatory pathways, upregulate immune-checkpoint (IC) molecules, and remodel the tumor microenvironment (TME) to favor immune escape. Paradoxically, their structural instability and aberrant accumulation generate tumor-specific neoepitopes, rendering mut-p53 a potential tumor-specific antigen (TSA) with both immunogenic and immunosuppressive properties. Such dual propensity of mut-p53 positions it as a central architect of immune editing and a critical predictor of immunotherapy outcomes. This review amalgamates growing molecular and clinical evidences to elucidate how mut-p53 regulates the immunogenic continuum of malignancies and contributes to foster immunotherapy resistance. Furthermore, this review emphasizes the novel therapeutic prospects of hotspot TP53 mutations in either generating neoantigen vaccines, T cell receptor (TCR)-based therapies, or by pharmacological targeting of mut-p53 to restore immune surveillance, improve antigen presentation, and synergize with immune-checkpoint blockade (ICB). By bridging the conceptual frameworks of tumor immunogenicity and oncogenic signaling, current review highlights mut-p53 as a promising context-dependent biomarker whose predictive value is determined by its interaction with established molecular and immunological determinants of tumor immunogenicity, immune escape, therapeutic resistance, and tumor evolution; thus underscoring its promise as both a biomarker and a therapeutic target in crafting next-generation precision cancer immunotherapy strategies. Dual immunological identity of mutant p53 (mut-p53) functions as the context-dependent determinant of tumor immunogenicity and cancer immunotherapy outcome. Mut-p53 exerts a context-dependent influence on anti-tumor immunity by functioning as both a driver of immune evasion and a potential source of tumor-specific neoepitopes. With the advancement of tumor stages, mut-p53 promotes reduced antigen processing and presentation, increased immune checkpoint signaling and T-cell exhaustion, secretion of tumor-derived immunomodulatory factors, and establishment of an immune-suppressive tumor microenvironment, thereby facilitating immune escape and limiting the efficacy of cancer immunotherapy as a negative modulator of the tumor microenvironment (TME). Conversely, in favorable molecular and immunological contexts, mut-p53-derived neoepitopes can enhance antigen presentation, stimulate tumor-specific T-cell activation, promote an inflamed TME, and facilitate immune-mediated tumor elimination as a tumor-specific antigen, resulting in improved responsiveness to immunotherapeutic interventions