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Background and Objective: Dengue fever (DF) has been a major health concern globally. Pakistan is also combating this infection for the last decade. Cytokine genes play an important role in DF pathogenesis. This study aimed to analyze dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and tumor necrosis factor α (TNF-α) genes promoter polymorphisms in DF patients. Methods: A total of 140 (n = 140) dDF patients were recruited for study at the Department of Human Genetics and Molecular Biology of University of Health Sciences, Lahore, Pakistan over a period of 3 years. Simple DF was noted in 105 patients (75%) while 35 (25%) showed bleeding complications. All patients were found positive for dengue non-structural protein or dengue IgM. All patients were tested for two polymorphisms in TNF-α (-238G/A, and -308G/A) and one polymorphism in DC-SIGN (-336G/A) using restriction fragment length polymorphism technique. A single nucleotide polymorphism stats program was used for statistical analysis. Results: Susceptibility to develop dengue infection in the presence of -336G allele odds ratio (OR = 27.95, p = Conclusion: This work suggests a potential association of DC-SIGN -336 polymorphism with susceptibility to develop symptomatic dengue illness. However, no potential association was found between TNF-α promoter polymorphisms and dengue infection in this study.

Background and Objective: Premature ovarian failure is a worldwide concern effecting 1% of females of reproductive age. The objective of the present study was to analyze the role of inhibin alpha (INHα) gene mutation (769G>A) in patients with premature ovarian failure (POF) in the local population. Methods: This case-control association studywas conducted in Department of Gynecology, Jinnah Hospital and The Children’s Hospital and Institute of Child Health from July 2015-July 2016. A total of n = 100 were recruited for this study and divided into two gropus females with equal number (n = 50)of patients andnormal controls of reproductive age (14 – 40 years). The screening of theINHα for 769G>A variation in exon 2 was done through DNA sequencing. Results: A higher frequency of the major allele G was seen in both the patients (99%) and the controls (87%) while comparing to minor allele A (1% in patients and 13% in controls). None of the patients was found to be homozygous (AA = 0%) for allele A, whereas, four of the controls were homozygous (AA = 8%). The frequency of the minor A allele in controls was found to be statistically significant (P-value = 0.002). Conclusion: An association of decreased risk of POFwith A allele of the 769G>A variant rather than increasing the risk of development of ovarian failure.

The infection caused by Severe Acute Respiratory Syndrome-Corona Virus 2 (SARS-CoV-2) has rapidly emerged as a serious pandemic, causing substantial morbidity and sometimes mortality with a significant healthcare burden. Unfortunately, Pakistan is among top twenty countries of the world affected by COVID19. The clinical spectrum in COVID-19 is diverse, ranging from mild disease having flu-like symptoms to potentially fatal ARDS, cytokine storm, multiple organ failure and death. Common risk factors associated with severe outcome in COVID-19 infection include male gender, older age and presence of comorbidities such as hypertension, diabetes and cardiovascular disease. Here we reviewed the available literature and report that the underlying mechanisms that account for a broad range of symptoms during respiratory viral infections, that have been well studied in the case of influenza viruses, adenoviruses, SARS-CoV and MERS-CoV, suggest that host genetic and epigenetic factors may also play a significant role in determining susceptibility and clinical outcome in COVID-19 infection. In this review we discuss the potential roles of host genetic factors including cellular receptors for COVID-19, HLA and inflammatory cytokine genes. Based on the SARS-CoV-2 genome and protein-protein interactions map between host and viral proteins we also describe the potential roles of several viral proteins in epigenetic modulation of host inflammatory innate immune response by targeting different cellular pathways particularly NF-κB activation, which may lead to the inflammatory cytokine storm and a severe COVID-19 disease. Investigations of these genetic and epigenetic mechanisms during COVID-19, especially in local settings, will be helpful in management of patients with higher risks and in the development of novel antiviral therapeutics.