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Of late, several cases of COVID-19-associated mucormycosis (CAM) are being reported worldwide. Although a causal link between COVID-19 and mucormycosis remains unearthed, multiple factors including glucocorticoids, worsening blood glucose control, ketoacidosis, increased serum-free iron (due to hyperferritinemia and acidosis), and viral-induced lymphopenia have been implicated in the pathogenesis of CAM.1 Notably, most of the cases of CAM have been reported from India.2 India, per se , has the highest burden of mucormycosis globally, with an estimated prevalence of 140 cases per million population. Besides, India is home to nearly 77 million people with diabetes; unarguably, diabetes mellitus is a major risk factor for mucormycosis.3 Nevertheless, there has been an unprecedented and alarming upsurge in the number of cases of CAM across several states, as the second wave of the COVID-19 pandemic continues to rampage in India. Until 19 May 2021, approximately 5500 people were affected with CAM in India, resulting in 126 casualties.4 Subsequently, CAM has been declared an epidemic disease in many states across the country. Amid this raging cataclysm, it is crucial to reflect on the possible reasons and ways to tide over the additional crisis of the ‘black fungus ’. As always, prevention is better than cure. …

The second wave of the COVID-19 pandemic has hit India hard. The number of new cases per day has gone up from 11 794 in the first week of February 2021 to over 414 000 as of 6 May 2021. The number of new deaths per day has shot up from 116 in the first week of February 2021 to more than 4500 as of 18 May 2021. Test positivity rates rose nationwide from 2.8% in the first week of April 2021 to 22% in the first week of May. The second wave is different from the first wave that occurred in September 2020 in a few ways. First, the rate of increase in new cases is significantly higher. Second, a marginal rise has been recorded in the number of young people testing positive for the virus than the first wave. Third, compared with the first wave, there has been a substantial increase in the proportion of patients presenting with shortness of breath and those requiring oxygen supplementation and mechanical ventilation during the ongoing second wave. The sudden avalanche of severe COVID-19 cases has expectedly led to an acute shortage of hospital beds, oxygen and medications. Finally, unlike the first wave, a significant proportion of the cases in the second wave are being caused by SARS-CoV-2 variants, which are believed to be more …

Purpose Observations studies have shown that prior use of statins is associated with a reduced risk of adverse clinical outcomes in patients with COVID-19. However, the available data are limited, inconsistent and conflicting. Besides, no randomised controlled trial exists in this regard. Hence, the present meta-analysis was conducted to provide an updated summary and collate the effect of statin use on clinical outcomes in COVID-19 using unadjusted and adjusted risk estimates. Methods PubMed, Scopus and Web of Science databases were systematically searched using appropriate keywords till December 18 2020, to identify observational studies reporting clinical outcomes in COVID-19 patients using statins versus those not using statins. Prior and in-hospital use of statins were considered. Study quality was assessed using the Newcastle-Ottawa Scale. Unadjusted and adjusted pooled odds ratio (OR) with 95% CIs were calculated. Results We included 14 observational studies pooling data retrieved from 19 988 patients with COVID-19. All the studies were of high/moderate quality. Pooled analysis of unadjusted data showed that statin use was not associated with improved clinical outcomes (OR 1.02; 95% CI 0.69 to 1.50, p=0.94, I2=94%, random-effects model). However, on pooling adjusted risk estimates, the use of statin was found to significantly reduce the risk of adverse outcomes (OR 0.51; 95% CI 0.41 to 0.63, p Conclusions Statin use is associated with improved clinical outcomes in patients with COVID-19. Individuals with multiple comorbidities on statin therapy should be encouraged to continue the drug amid the ongoing pandemic.

Similar to the SARS-CoV experience,1 a possible link between ABO blood groups with COVID-19 susceptibility and severity has been shown in multiple observational studies.2–4 Gerard et al 5 have further noted that people with B and/or O blood groups were less represented among COVID-19 patients, thereby highlighting the possible beneficial role of anti-A antibodies in COVID-19 susceptibility. In fact, it was known that anti-A antibodies can block the adhesion of SARS-CoV S-protein to ACE2 expressing cell lines.6 Given the genomic similarity between SARS-CoV-2 and SARS-CoV, it might be prudent to hypothesise a protective role of anti-A antibodies against COVID-19 severity as well. However, existing clinical evidence in this regard is controversial. Hoiland et al 7 had reported that critically ill COVID-19 patients with blood groups A and AB (lacking anti-A antibodies) were more likely to require mechanical ventilation and prolonged intensive care compared with patients with B/O (with anti-A antibodies). However, a genomewide association study of severe COVID-19 patients showed that those with blood group A had a higher risk of severe disease, while blood group O had a protective effect.8 Other studies found no association between ABO blood groups and COVID-19 severity/mortality.9–12 We aimed to summarise the available literature and provide a pooled analysis of the effect of A/AB (without anti-A antibodies) on clinical …

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has scourged the world ever since its outbreak in December 2019, affecting over three million people and claiming more than 207 000 lives over 200 countries all over the globe. Human-to-human transmission of SARS-CoV-2 occurs primarily by fomites and by respiratory droplets. This has, in turn, fanned public concerns that cash and coins could transmit the virus as well. Central banks have reported a surge in the number of queries from the media on the safety of using cash. Internet searches pertaining to both ‘cash’ and ‘virus’ or ‘COVID’ is at an all-time high.1 The apprehensions have been fuelled by studies that have demonstrated the remarkable stability of SARS-CoV-2 on inanimate objects and surfaces.2 Hence, we have summarised the possibilities of transmission of COVID-19 via currency and the feasible alternatives amid the prevailing circumstances. 1. Does viral transmission occur through cash and coins? Hitherto available in vitro data do suggest that human-to-human transmission of COVID-19 via cash and coins seems possible. SARS-CoV-2 has been shown to be more stable on smooth surfaces, and a detectable level of infectious virus has been recovered from banknotes and stainless steel (coins) even after 2 and 4 days of inoculation, respectively. In addition, a biphasic decay of infectious SARS-CoV-2 has been found in samples recovered from smooth surfaces, thereby further prolonging the duration of stay of the virus.3 However, recovery of the virus from inoculated objects in in vitro often requires elution of the virus by …