Background: The disease severity, ranging from being asymptomatic to having acute illness, and associated inflammatory responses has suggested that alterations in the gut microbiota may play a crucial role in the development of chronic disorders due to COVID-19 infection. This study describes gut microbiota dysbiosis in COVID-19 patients and its implications relating to the disease. Design: A cross sectional prospective study was performed on thirty RT-PCR-confirmed COVID-19 patients admitted to the All India Institute of Medical Sciences, Bhopal, India, between September 10 and 20, 2020. Ten healthy volunteers were recruited as the control group. IFN, TNF, and IL-21 profiling was conducted using plasma samples, and gut bacterial analysis was performed after obtaining the metagenomics data of stool samples. Results: Patients with a variable COVID-19 severity showed distinct gut microflora and peripheral interleukin-21 levels. A low Firmicute/Bacteroidetes ratio, caused by the depletion of the fibre-utilizing bacteria, F. prausnitzii, B. Plebius, and Prevotella, and an increase in Bacteroidetes has associated gut microbiota dysbiosis with COVID-19 disease severity. Conclusions: The loss of the functional attributes of signature commensals in the gut, due to dysbiosis, is a predisposing factor of COVID-19 pathophysiology.

Background. The epidemiology of human papilloma virus (HPV) infection and the pattern of HPV genotype distribution are much-needed parameters to assess the risk of cervical cancer among females. However, due to less availability of data on HPV burden and its genotypes from various geographical regions in India makes cervical cancer screening modalities and vaccination strategies difficult to implement. Objective. The present study was conducted to identify the various genotypes particularly high-risk HPV types in premalignant or malignant cervical lesions. Methods. The study was a hospital-based cross-sectional study wherein 295 symptomatic women were screened by Pap smear and multiplex real-time PCR was performed for HPV genotypes identification in women with abnormal cervical cytology. Results. Out of 295 women, 237 (80.3%), 45 (15.3%), and 13 (4.4%) women had normal Pap smear, squamous cell carcinoma and precancerous cytology, respectively. Among these 58 women having abnormal cervical cytology, HPV was detected in 48 (81.0%) participants. Most common HPV genotypes in our study were HPV 16 ( n = 29 ; 60.4%) followed by mixed infections; i.e., more than one type of HPV was detected ( n = 10 , 20.8%). HPV 18 was detected only in 6.25%, whereas other high-risk HPV genotypes were found to be 12.5%. Conclusion. HPV positivity was >80% in women having abnormal Pap smear. The prevalence of HPV 18 was found to be much less in Central India, compared to other parts of country. HPV 16 was the most common genotype followed by mixed HPV genotype infections. It is evident from our study that symptomatic women even if having normal Pap smear should be screened for HPV and followed up with periodic Pap smears for detecting any change in cervical cytology, thus preventing cervical cancer in women.

The transplacental route of vertical transmission of Hepatitis B Virus (HBV) has been known for over a decade. Here we present evidence which suggest HBV can replicate in placenta. Forty-one HBsAg positive and 10 control pregnant women were enrolled in the study after obtaining informed consent. HBV positives were further divided in the High Viral Load (HVL) Group and Low Viral Load (LVL) Group according to INASL guidelines 2018. The Presence of the HBV DNA and expression of NTCP in the placenta was analyzed by qPCR/RT-qPCR and/or immunohistochemistry (IHC). The presence of cccDNA was assessed using Digital Droplet PCR while the presence of pre-genomic (pg) RNA was assessed through qRT-PCR and sequencing. The presence of HBeAg and HBcAg in the placenta was assessed by IHC. Immunostaining of NTCP, HBeAg and HBcAg on trophoblasts along with the presence of total HBV DNA, cccDNA and pgRNA indicated, that these cells are not only susceptible to HBV infection but may also support viral replication. This is further supported by the finding that trophoblasts of the several HBeAg seronegative samples harbored the HBeAg. Although, we did not find any correlation in NTCP expression and viral markers with viral load indicates placental replication may not aping hepatocytes. The presence of the HBV receptor, NTCP along with the presence of cccDNA, pgRNA, and HBeAg in placenta of HBV infected females without circulating HBeAg suggest that placenta act as a replication host.

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