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This year, some highly transmissible variants of COVID-19 has led to devastating health crisis is many parts of the world. India is one of the worst affected countries with sudden and alarming surge in cases in April-May. However, the situation in the country is now under control and cases have also significantly come down. Scientists are studying the various strains of the novel coronavirus in an attempt to understand just how dangerous or benign they may be. They have found that some are highly infectious while others are not dangerous at all. Now, a new study at the Johns Hopkins School of Medicine have found that while Alpha and Beta COVID-19 variants are associated with higher transmission, patients with these variants show no evidence of higher viral loads in their upper respiratory tracts when compared to the control group.
It is a fact that the emergence and higher transmission of the evolving variants of SARS-CoV-2, the virus that causes COVID-19, has been concerning indeed. For the new study, the researchers analysed Alpa (B117), the variant that was first identified in the UK, and Beta (B1351), which emerged out of South Africa. Their aim was to evaluate if patients showed higher viral loads, and consequently increased shedding and transmissibility if infected with these variants. However, researchers were not able to establish why exactly these variants show higher transmissibility.
During the course of their investigation, researchers found that patients infected with these two variants of COVID-19 are less likely to be asymptomatic when compared to the control group. They also saw that although those infected with the variants were not at higher risk for death or intensive care admission, they were more likely to be hospitalised.
Researchers identified the variants by using whole genome sequencing. They used a large cohort of samples to show that the UK variant constituted 75 per cent of the circulating viruses by April 2021. They also compared 134 variant samples to 126 control samples and, with access to the patients' clinical information, were able to correlate the genomics data with the clinical disease and outcomes. All samples were scrutinised minutely and put through additional testing to determine their viral load. The information was associated with the stage of the disease by looking at the days after the start of symptoms. This added clarity in comparing viral shedding between groups.
(With inputs from IANS)