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The risk for community acquired pneumonia (CAP) is partially driven by genetics. To identify the CAP-associated genetic risk loci, we performed a meta-analysis of clinically diagnosed CAP (3,310 individuals) with 2,655 healthy controls. The findings revealed CYP1A1 variants (rs2606345, rs4646903, rs1048943) associated with pneumonia. We observed rs2606345 [G vs T; OR=1.49(1.29-1.69); p=0.0001; I2= 15.5%], and rs1048943 [T vs G; OR= 1.31(0.90-1.71); p=0.002; I2=19.3%] as risk markers and rs4646903 [T vs C; OR= 0.79(0.62-0.96); p=0.03; I2=0%] as a protective marker for susceptibility to CAP, when compared with healthy controls. Our meta-analysis showed the presence of CYP1A1 SNP alleles contributing significant risk toward pneumonia susceptibility. Interestingly, we observed a striking difference of allele frequency for rs2606345 (CYP1A1) among Europeans, Africans and Asians which may provide a possible link for observed variations in death due to coronavirus disease 2019 (COVID-19), a viral pneumonia. We report, for the first time, a significant positive correlation for the risk allele (T or A) of rs2606345, with a higher COVID-19 mortality rate worldwide and within a genetically heterogeneous nation like India. Mechanistically, the risk allele ‘A’ (rs2606345) is associated with lower expression of CYP1A1 and presumably leads to reduced capacity for xenobiotic detoxification. We note that ambient air pollution, a powerful inducer of CYP1A1 gene expression, is globally associated with lower, not higher mortality, as would normally be predicted. In conclusion, we find that CYP1A1 alleles are associated with CAP mortality, presumably via altered xenobiotic metabolism. We speculate that gene-environment interactions governing CYP1A1 expression may influence COVID-19 mortality.

© 2017 Blackwell Verlag GmbH Foot-and-mouth disease (FMD) is, arguably, the animal disease with the most devastating global economic impact owing in part, to the severe trade restrictions imposed upon affected countries and regions. South Asia is one of the regions where widespread lineages of the FMDV virus (FMDV) have emerged. Here, we performed an integrative phylogenetic analysis of all FMDV serotypes (A, O and Asia-1) circulating in southern Asia, including viral sequences collected until 2013. Our results describe the occurrence of FMD caused by different serotypes and lineages, focusing in the cycles where a specific lineage predominates within a region for a protracted period and then are rapidly or progressively replaced by an emergent or re-emergent strain that is introduced from an adjacent region. Transmission between the two main regions in southern Asia (the Indian subcontinent and the region comprised by Afghanistan, Iran and Pakistan) has been limited. Results of time divergence estimation of lineages that currently circulate in this region indicate that the most recent common ancestor of endemic lineages are: 1992 [1989–1995] for lineage O/PanAsia; 1997 [1995–1999] for PanAsia2; 2001 [1998–2004] for O/Ind2001; 2001 [2000–2002] for A/Iran-05; 1990 [1988–1991] for A/G-18 (G-VII); 2003 [2000–2006] for Asia-1 Sindh08 and 2002 [1999–2004] for Asia-1 G-VIII. We estimated the mean of the overall substitution rate of the VP1 coding region (substitution/site/year) for serotype O (5.95 × 10−3), serotype A (1.19 × 10−2) and serotype Asia-1 (3.08 × 10−3). The potential factors driving the lineage turnover are discussed. Our results provide insights into the ecological and evolutionary factors driving the emergence of FMDV.

The paradigmatic, fatal and devastating ailment called avian influenza or bird flu is a highly contagious viral disease caused by type A influenza virus, It primarily affects the respiratory, digestive and/or nervous system of chickens, turkeys, guinea fowls and other avian species and less commonly pigs and other species of mammals including human. In India, The first pandemic outbreak of Avian Influenza was reported during 2006. In this study, we selected an isolate of high pathogenic avian influenza (A/Ck/Jalgaon/India/12419/2006) H5N1 virus and propagated in chicken embryo fibroblast. Later this virus was adopted and propagated in Madin-Darby canine kidney cells (MDCK) and Vero cells. Infected non-avian cells with an avian virus shown cytopathic effects like rounding, cytoplasmic elongation, syncytia formation and later stages fluffing from the attached surface. The harvested virus suspension shown increased haemagglutination titre (HA) than viral suspension from chicken embryo fibroblast culture and the presence of virus was confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR). The obtained result reveals that virus had capacity to adopt for the invitro culture and propagate in non avian host cells with higher titre. This infers the chance of virus to cross the host barrier and probable chance of infection in human being.

A 45-year-old male patient presented with gradual onset of headache, vomiting and blurring of vision of 28 days duration. Ophthalmological examination revealed normal anterior segment and pupillary reflex. No abnormality was detected in the vitreous. Optic disc showed features of advanced papilledema with normal macula and retinal periphery in both eyes. Visual acuity was 20/200 in the right eye and counting fingers close range in the left eye. Non-contrast computed tomography of brain was normal and magnetic resonance imaging showed sagittal sinus thrombosis without any evidence of venous infarction or intracranial mass. Routine hematological investigations revealed increased hemoglobin level, packed cell volume and leucocytosis. Further investigation revealed increased Vitamin B12 and decreased serum erythropoietin. A diagnosis of polycythemia vera was made from the above findings. This case is being presented for the rarity of association of polycythemia vera with bilateral advanced papilledema due to sagittal sinus thrombosis.