Severe acute respiratory syndrome‐coronavirus‐2 (SARS‐CoV‐2) infection causes coronavirus disease‐19 (COVID‐19), which is characterized by clinical manifestations such as pneumonia, lymphopenia, severe acute respiratory distress, and cytokine storm. S glycoprotein of SARS‐CoV‐2 binds to angiotensin‐converting enzyme II (ACE‐II) to enter into the lungs through membrane proteases consequently inflicting the extensive viral load through rapid replication mechanisms. Despite several research efforts, challenges in COVID‐19 management still persist at various levels that include (a) availability of a low cost and rapid self‐screening test, (b) lack of an effective vaccine which works against multiple variants of SARS‐CoV‐2, and (c) lack of a potent drug that can reduce the complications of COVID‐19. The development of vaccines against SARS‐CoV‐2 is a complicated process due to the emergence of mutant variants with greater virulence and their ability to invoke intricate lung pathophysiology. Moreover, the lack of a thorough understanding about the virus transmission mechanisms and complete pathogenesis of SARS‐CoV‐2 is making it hard for medical scientists to develop a better strategy to prevent the spread of the virus and design a clinically viable vaccine to protect individuals from being infected. A recent report has tested the hypothesis of T cell immunity and found effective when compared to the antibody response in agammaglobulinemic patients. Understanding SARS‐CoV‐2‐induced changes such as “Th‐2 immunopathological variations, mononuclear cell & eosinophil infiltration of the lung and antibody‐dependent enhancement (ADE)” in COVID‐19 patients provides key insights to develop potential therapeutic interventions for immediate clinical management. Therefore, in this review, we have described the details of rapid detection methods of SARS‐CoV‐2 using molecular and serological tests and addressed different therapeutic modalities used for the treatment of COVID‐19 patients. In addition, the current challenges against the development of vaccines for SARS‐CoV‐2 are also briefly described in this article.

Despite a thorough understanding of the structure of human papillomavirus (HPV) and its genotypic variations (high-risk and low-risk variants), the mechanisms underlying HPV-induced cervical cancer (CC) pathogenesis and the molecular signatures of drug resistance remain to be fully understood. Accumulating evidence has shown the involvement of kinase targets in the induction of drug resistance in high-risk (HR) HPV-CC. Molecularly, the genome of high-risk HPV is reported to control the expression of host kinases. In particular, Aurora kinases A, B, and C (ARKA, ARKB, and ARKC), phosphotidylinositol–trisphosphate kinase (PI3K)-Akt, and Glycogen synthase kinase3-α/β (GSK3 α/β) promote the transformation of infected cells, and also enhance the resistance of cells to various chemotherapeutic agents such as nelfinavir and cisplatin. However, the precise mechanisms through which HPV activates these kinases are yet to be fully elucidated. Furthermore, there is still ambiguity surrounding whether targeting HPV-induced kinases along with HPV-targeted therapies (such as phytopharmaceuticals and PROTAC/CRISPR-CAS-based systems) synergistically inhibit cervical tumor growth. Given the critical role of kinases in the pathogenesis and treatment of CC, a comprehensive review of current evidence is warranted. This review aims to provide key insights into the mechanisms of HPV-induced CC development, the involvement of kinases in drug resistance induction, and the rationale for combination therapies to improve clinical outcomes.

Background/Objectives: Asthma is a heterogeneous inflammatory airway disease. Periostin, a matricellular protein induced by interleukin-13, contributes to airway inflammation and remodeling. This study evaluated serum periostin as a diagnostic biomarker and explored multidimensional phenotypes in adult asthma. Methods: A cross-sectional study included 76 adults, with 25 healthy controls, 25 moderate, and 26 severe asthma patients, classified per Global Initiative for Asthma (GINA)-2020 guidelines. Serum periostin was measured using an enzyme-linked immunosorbent assay (ELISA). Diagnostic accuracy was assessed using receiver operating characteristic (ROC) analysis, Firth-penalized logistic regression, bootstrap calibration (1000 resamples), decision curve analysis (DCA), and gradient boosting machine (GBM) validation. Principal component analysis (PCA) followed by k-means clustering identified distinct phenotypes based on clinical, functional, and inflammatory variables. Results: Asthma patients had higher serum periostin than controls (median 52.9 vs. 32.5 pg/mL; p < 0.01), with excellent diagnostic accuracy (AUC = 0.987; sensitivity = 94.1%, specificity = 100%). Firth regression identified periostin as the only independent predictor of asthma diagnosis (β = 0.387; OR = 1.47; 95% CI 1.23–2.08; p < 0.001). Calibration showed minimal error (MAE = 0.042) and DCA demonstrated clear net benefit. GBM confirmed periostin as the dominant diagnostic predictor. PCA revealed three clusters: Cluster 1: younger, lower periostin, preserved lung function, good symptom control; Cluster 2: intermediate periostin, greater airflow limitation, poorer control; and Cluster 3: highest periostin, elevated systemic inflammation (NLR, PLR, SII), with moderate functional impairment. Conclusions: Serum periostin is a reliable diagnostic biomarker for asthma. Multidimensional clustering highlights clinically relevant phenotypes linked to periostin, inflammatory burden, and lung function, supporting its role in personalized asthma management.

Background: Chronic Obstructive Pulmonary Disease (COPD) remains a leading cause of morbidity and mortality worldwide, particularly in low- and middle-income countries (LMICs), where both tobacco and biomass smoke exposure are major risk factors. While spirometry is the diagnostic gold standard, reliable non-invasive biomarkers are needed for early detection and disease monitoring. The soluble receptor for advanced glycation end-products (sRAGE), a circulating decoy receptor with anti-inflammatory activity, has shown potential in this context. Methods: In this prospective, exposure-stratified, cross-sectional study, 150 adults were enrolled into four groups of 25 each—tobacco-smoke COPD, male tobacco-exposed controls, biomass-smoke COPD, and female biomass-exposed controls—along with 50 healthy controls (25 males, 25 females). Participants underwent clinical evaluation, spirometry, and serum sRAGE quantification (ELISA). Systemic inflammation was assessed using neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR). Correlation and receiver operating characteristic (ROC) analyses determined diagnostic performance. Results: Serum sRAGE levels were significantly lower in tobacco-induced (545 ng/mL) and biomass-induced COPD (540 ng/mL) versus controls (1207–1462 ng/mL; p < 0.001). sRAGE correlated positively with FEV₁, FVC, and FEV₁/FVC (r = 0.54–0.75, p < 0.001), and negatively with CAT, mMRC, and SGRQ-C. ROC analysis showed excellent discrimination (AUC = 0.990; 94% sensitivity; 96% specificity at 946 ng/mL cutoff). Conclusions: Serum sRAGE is a robust, non-invasive biomarker for COPD diagnosis and severity assessment across exposure phenotypes. Its integration into clinical practice may enhance early detection and risk stratification, particularly in LMICs.

Background: Tuberculosis (TB) is a global health burden caused by Mycobacterium tuberculosis (Mtb) infection. Fibronectin (Fn) facilitates Mtb attachment to host cells. We studied the Fn levels in smear-positive TB patients to assess its correlation with disease severity based on sputum smears and chest X-rays. Methods: Newly detected consecutive sputum AFB-positive pulmonary TB patients (n = 78) and healthy control subjects (n = 11) were included. The mycobacterial load in the sputum smear was assessed by IUATLD classification, ranging from 0 to 3. The severity of pulmonary involvement was assessed radiologically in terms of both the number of zones involved (0–6) and as localized (up to 2 zones), moderate (3–4 zones), or extensive (5–6 zones). The serum human fibronectin levels were measured by using a commercially available enzyme-linked immunosorbent assay (ELISA) kit (Catalogue No: CK-bio-11486, Shanghai Coon Koon Biotech Co., Ltd., Shanghai, China). Results: The PTB patients showed lower Fn levels (102.4 ± 26.7) compared with the controls (108.8 ± 6.8), but they were not statistically significant. Higher AFB smear grades had lower Fn levels. The chest X-ray zones involved were inversely correlated with Fn levels. The Fn levels, adjusted for age and gender, decreased with increased mycobacterial load and the number of chest radiograph zones affected. A Fn level <109.39 g/mL predicted greater TB severity (sensitivity of 67.57% and specificity of 90.38%), while a level <99.32 pg/mL predicted severity based on the chest radiology (sensitivity of 84.21% and specificity of 100%). Conclusions: The Fn levels are lower in tuberculosis patients and are negatively correlated with severity based on sputum mycobacterial load and chest radiographs. The Fn levels may serve as a potential biomarker for assessing TB severity, which could have implications for early diagnosis and treatment monitoring.