Virus World

Following the emergence of SARS-CoV-2 in China in late 2019 a number of variants have emerged, with two of these – Alpha and Delta – subsequently growing to global prevalence. One characteristic of these variants are changes within the Spike protein, in particular the receptor binding domain (RBD). From a public health perspective these changes have important implications for increased transmissibility and immune escape; however, their presence could also modify the intrinsic host-range of the virus. Using viral pseudotyping we examined whether the variants of concern (VOCs) Alpha, Beta, Gamma and Delta have differing host ACE2 receptor usage patterns, focusing on a range of relevant mammalian ACE2 proteins. All four VOCs were able to overcome a previous restriction for mouse ACE2, with demonstrable differences also seen for individual VOCs with rat, ferret or civet ACE2 receptors, changes which we subsequently attribute to N501Y and E484K substitutions within the Spike RBD.

Preprint Available in bioRxiv (Nov. 24, 2021):

https://doi.org/10.1101/2021.11.23.469663

Background

The B.1.617.2 (delta) variant of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (Covid-19), has contributed to a surge in cases in India and has now been detected across the globe, including a notable increase in cases in the United Kingdom. The effectiveness of the BNT162b2 and ChAdOx1 nCoV-19 vaccines against this variant has been unclear.

Methods

We used a test-negative case–control design to estimate the effectiveness of vaccination against symptomatic disease caused by the delta variant or the predominant strain (B.1.1.7, or alpha variant) over the period that the delta variant began circulating. Variants were identified with the use of sequencing and on the basis of the spike (S) gene status. Data on all symptomatic sequenced cases of Covid-19 in England were used to estimate the proportion of cases with either variant according to the patients’ vaccination status.

Results

Effectiveness after one dose of vaccine (BNT162b2 or ChAdOx1 nCoV-19) was notably lower among persons with the delta variant (30.7%; 95% confidence interval [CI], 25.2 to 35.7) than among those with the alpha variant (48.7%; 95% CI, 45.5 to 51.7); the results were similar for both vaccines. With the BNT162b2 vaccine, the effectiveness of two doses was 93.7% (95% CI, 91.6 to 95.3) among persons with the alpha variant and 88.0% (95% CI, 85.3 to 90.1) among those with the delta variant. With the ChAdOx1 nCoV-19 vaccine, the effectiveness of two doses was 74.5% (95% CI, 68.4 to 79.4) among persons with the alpha variant and 67.0% (95% CI, 61.3 to 71.8) among those with the delta variant.

Conclusions

Only modest differences in vaccine effectiveness were noted with the delta variant as compared with the alpha variant after the receipt of two vaccine doses. Absolute differences in vaccine effectiveness were more marked after the receipt of the first dose. This finding would support efforts to maximize vaccine uptake with two doses among vulnerable populations. (Funded by Public Health England.)

Published in NEJM (July 21, 2021):

https://doi.org/10.1056/NEJMoa2108891 

A new study adds to growing evidence suggesting that the Delta coronavirus variant is not only highly transmissible, but also more dangerous.  Covid-19 patients infected with the Delta variant had about double the risk of hospitalization compared to those infected with the Alpha variant, according to the study published Friday in the journal Lancet Infectious Diseases. "The results suggest that patients with the Delta variant had more than two times the risk of hospital admission compared with patients with the Alpha variant," researchers from Public Health England and the University of Cambridge wrote in their new study. "Emergency care attendance combined with hospital admission was also higher for patients with the Delta variant, showing increased use of emergency care services as well as inpatient hospitalization," the researchers wrote.

And what that tells us about the pandemic. Like any virus, SARS-CoV-2 has been mutating constantly since the beginning of the pandemic. Until November 2020, though, that didn’t seem to matter. That’s when scientists in the United Kingdom noticed an alarming change: The virus had mutated in a way that made it more transmissible. Within a month, similar reports were emerging from places around the world. Suddenly, it seemed the virus was changing at an alarming rate. SARS-CoV-2 hasn’t actually been mutating faster, though. Instead, by letting it spread around the world, we’ve just given it more and more opportunities to mutate as it replicates. The result is that after countless random mutations, there are signs that the virus is beginning to adapt to our natural defenses. And because it’s completely normal for a virus to change over time, we shouldn’t expect it to stop. The only real way to stop those changes is to stop giving the virus so many opportunities.

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