SARS-CoV-2 Delta strain

    Posted on Sep 13, 2021

    In a classic case of Darwinian selection, the successful Delta variant (B.1.617.2) has largely displaced all other forms of the coronavirus underlying the ongoing global pandemic. The relatively large pool of unvaccinated persons (either from choice in developed countries or lack of vaccine availability elsewhere) has certainly contributed to the speed with which variants have arisen. However, the emergence of more competitive versions of the SARS-CoV-2 virus was an evolutionary inevitability. Mutations occur randomly; those that offer a competitive advantage are maintained and propagated within a species’ population.

    Based on recent estimates, the Delta strain may be over twice as infectious as the original strain of SARSCoV-2. While aspect may be contributing to an apparent increase in breakthrough infections in the vaccinated population, the overwhelming proportion of infections reported in the US are occurring in the unvaccinated. According to a recent Kaiser Family Foundation survey of 25 US states reporting data on breakthrough infections (https://www.kff.org/policy-watch/), the rate of cases reported among the fully vaccinated is well below 1% in all reporting states, ranging from 0.01% in Connecticut to 0.29% in Alaska. Because of the high proportion of asymptomatic, undiagnosed cases in the younger unvaccinated population, the proportion of breakthrough infections may be even lower. Hospitalization rates reported for fully vaccinated individuals in the survey ranged from 0.06% in Arkansas to effectively zero in California, Delaware, District of Columbia, Indiana, New Jersey, New Mexico, Vermont, and Virginia, indicating that the existing vaccines are still highly protective against the new dominant strain even when breakthrough infections occur.

    Considerable research has been conducted to determine why the Delta variant has been so successful. Many of these studies are currently only available as pre-prints because of the necessarily measured pace of peer review. Some of the papers offer contradictory assessments of the lethality/severity of Delta variant infections relative to those from other strains. Because experienced, knowledgeable researchers presently disagree on the issue, it is premature to draw definitive conclusions. However, some very interesting pieces of evidence have been presented on exactly how the Delta variant manages to be so transmissible.

    For example, a paper from Guangzhou, China by Li et al., (https://doi.org/10.1101/2021.07.07.21260122) indicates that the Delta strain leads to higher levels of virus in the respiratory tract, where presumably larger numbers of viral particles would then be expelled to infect others. In a study of 62 persons infected with the Delta variant, back-of-throat swab samples taken daily had over 1000-fold higher levels of SARSCoV-2 RNA at their first positive test than in 63 individuals with other strains. Additionally, the Delta-infected subjects tested positive in an average of just four days after viral exposure compared with six days for those infected with other variants. The combination of a shorter incubation period with higher numbers of virus particles could underlie the increased infectiousness seen with the Delta variant. Moreover, a shorter incubation period increases the difficulty of contact tracing in countries that systematically track and quarantine infected individual’s contacts.

    In terms of determining a mechanism for how such increases in viral load might occur, a particular mutation (P681R) found in the Delta variant at the so-called furin cleavage site has drawn interest. This site is situated at the junction of the two subunits of the SARS-CoV-2 spike protein, the piece of the virus particle that binds to the human ACE2 receptor as a means of infecting cells. The spike protein needs to be cleaved twice by host proteins before it can enter. One of these host proteins is furin. According to research in a recent preprint by Liu et al., (https://doi.org/10.1101/2021.08.12.456173) at the University of Texas Medical Branch (UTMB) in Galveston, TX, the P681R substitution of an arginine residue at this position allows furin cleavage to proceed more efficiently than in strains lacking the mutation, presumably contributing to more virus particles in the respiratory tract and higher infectivity as a result. There is some disagreement among researchers in the field on the extent to which this mutation contributes to the increased viral load observed in Delta strain infections. However, although the Delta variant bears additional distinctive mutations not only on its spike protein but in other genomic locations, none of these has yet emerged as an explanation as to why Delta is so much more infectious than other strains.

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