Background: Since the first reported outbreak of dengue hemorrhagic fever in Pakistan, several mini outbreaks have erupted in the region. Dengue virus serotype 3 (DEN-3) was first documented in 2005 outbreak in Karachi. Reports show that serotype 3 is prevalent in Lahore since 2008. Serotype 2 (DEN-2) is the major circulating serotype in Pakistan as it is documented since 1994. We have conducted a detailed study of three outbreaks of dengue virus infection that occurred in years 2007, 2008 and 2009 in Lahore by using molecular techniques such as PCR and nucleotide sequencing of the C-prM gene junction of Dengue virus. Results: Through the analysis of 114 serum samples collected over the period of three years (2007-2009), total 20 patients were found to be infected with dengue virus. In year 2007, four were positive for serotype 2 and one sample was positive for serotype DEN-3. In 2008, five samples had concurrent infection with serotypes DEN-2 and DEN-3 while three samples were infected only with serotype DEN-2. In year 2009, one sample had concurrent infection with serotypes DEN-2 and DEN-3 while six were positive for serotype DEN-2 only. Conclusions: Our study showed that serotype DEN-2 was dominant in positive samples of dengue virus infection collected during the period of three years (2007-2009). The other serotype present was serotype DEN-3. Genotypes of serotype DEN-2 and serotype DEN-3 were subtype IV and subtype III, respectively.

Hepatitis C virus is a major cause of chronic liver diseases which can lead to permanent liver damage, hepatocellular carcinoma and death. The presently available treatment with interferon plus ribavirin, has limited benefits due to adverse side effects such as anemia, depression and "flu-like" symptoms. Needless to mention, the effectiveness of interferon therapy is predominantly, if not exclusively, limited to virus type 3a and 3b whereas in Europe and North America the majority of viral type is 1a and 2a. Due to the limited efficiency of current therapy, RNA interference (RNAi) a novel regulatory and powerful silencing approach for molecular therapeutics through a sequence-specific RNA degradation process represents an alternative option. Several reports have indicated the efficiency and specificity of synthetic and vector based siRNAs inhibiting HCV replication. In the present review, we focused that combination of siRNAs against virus and host genes will be a better option to treat HCV

Helicobacter pylori is a gastric pathogen that induces chronic gastritis, which may progress to neutrophilic activity, glandular atrophy, intestinal metaplasia, and gastric carcinoma. The aim of this study was to evaluate H. pylori-induced tissue damage. A total of 602 gastric biopsy samples were collected, categorized, and analyzed using hematoxylin and eosin and Giemsa staining, followed by molecular confirmation through PCR targeting the species-specific 16S rRNA gene. H. pylori density and histopathological features were evaluated and graded according to the updated Sydney classification system. H. pylori was detected in 55% (n = 334) of cases, and the antrum (50.83%, p < 0.00001) was the predominant site. A slightly higher prevalence was observed in females, accounting for 56.9% compared to males at 43.1%, which was attributed to sociocultural exposure differences. Individuals aged 11–40 years accounted for 58.3% (n = 195), highlighting early-age acquisition of infection. H. pylori infection was significantly linked to moderate-to-severe inflammation (63.2%, p < 0.00001) and neutrophilic activity (53.3%, p < 0.00001). Intestinal metaplasia and atrophy were infrequent, present in 0.6% (95% CI, 0.02, p = 0.149) and 0.9% (95% CI, 0.05, p = 0.430) of individuals. H. pylori infection causes chronic inflammation and neutrophilic infiltration of the stomach mucosa. Early identification and histopathological examination are essential in assessing H. pylori-related gastric pathology.

Background: Hepatitis C Virus (HCV) remains a global health threat, causing severe liver diseases such as cirrhosis and hepatocellular carcinoma. Protein sequences are essential for exploring genetic variability and improving detection. This study presents a generative LSTM model, AI-VNA, for generating and analyzing NS5A protein sequences to enhance understanding of sequence diversity and improve predictive modeling. Methods: The AI-VNA model was trained on curated NS5A protein sequences and evaluated against baseline models including CNN, 1D-CNN, GRU, and Simple RNN. Generated sequences were validated using BLAST (version 2.16.0) to assess biological relevance. Additional analyses included a sequence similarity heatmap, phylogenetic clustering using UPGMA, and statistical comparison of sequence similarities via the Mann–Whitney U test. Results: AI-VNA achieved 98.56% accuracy, outperforming other models and demonstrating strong capability in modeling sequence patterns. BLAST validation showed an average query coverage of 82%, an average E-value of 1 × 10⁻¹⁵⁵, and 96.68% identity to known NS5A proteins. The sequence similarity heatmap revealed notable variability among the generated sequences. Phylogenetic analysis showed distinct clustering patterns, indicating both conservation and diversity. A box plot comparing similarity scores of predicted and database sequences showed significant variation (p = 0.01221; Cliff’s Delta = 0.291, small effect). Conclusions: These findings highlight the AI-VNA model’s ability to generate evolutionarily relevant and diverse NS5A protein sequences, supporting its potential for improving HCV sequence analysis and aiding in diagnostic and therapeutic developments.