Studies done at the University of Liverpool with K18-hACE2 mice shows that the Omicron variant is less severe.
(Note : The K18-hACE2 transgenic mice express human ACE2, the receptor used by SARS-CoV to gain entry to cells. The human keratin 18 (KRT18) promoter directs expression to epithelia, including airway epithelial cells where infections typically begin. This model of lethal infection with SARS-CoV mimics the human SARS-Cov pathogenesis.)
The mice were infected with the Pango B lineage, Delta, and Omicron variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the pathogenesis and viral loads of the variants were compared.
The results show that the Omicron variant had lower viral loads in both the lower and upper respiratory tracts than the other variants, at least in this mouse model. If this is the case in humans, other factors such as binding effectiveness to host cells, avoiding initial host defenses in contacts, and/or behavioral patterns must account for the high rate of transmission of the Omicron variant.
This implies that the Omicron variant may cause a less severe and/or faster recovery from clinical disease. However, given the high transmissibility of the Omicron variant and the fact that it evades much of the population's pre-existing immunity and existing antibody-based therapies, other measures such as social distancing, mask-wearing, and indoor contact restriction should be maintained to avoid a potentially disastrous impact on healthcare saturation.
PS: The Neyts Lab at Leuven University in Belgium found that in Syrian hamsters, with a lower viral load in the lungs compared with other variants. But Prof Johan Neyts said this may be because the virus was better at infecting humans than hamsters, or that it was more likely to infect the upper respiratory tract, or that it provoked less-severe disease.
Also another study in the US using mice also shows similar results.
(Note : The K18-hACE2 transgenic mice express human ACE2, the receptor used by SARS-CoV to gain entry to cells. The human keratin 18 (KRT18) promoter directs expression to epithelia, including airway epithelial cells where infections typically begin. This model of lethal infection with SARS-CoV mimics the human SARS-Cov pathogenesis.)
The mice were infected with the Pango B lineage, Delta, and Omicron variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the pathogenesis and viral loads of the variants were compared.
The results show that the Omicron variant had lower viral loads in both the lower and upper respiratory tracts than the other variants, at least in this mouse model. If this is the case in humans, other factors such as binding effectiveness to host cells, avoiding initial host defenses in contacts, and/or behavioral patterns must account for the high rate of transmission of the Omicron variant.
This implies that the Omicron variant may cause a less severe and/or faster recovery from clinical disease. However, given the high transmissibility of the Omicron variant and the fact that it evades much of the population's pre-existing immunity and existing antibody-based therapies, other measures such as social distancing, mask-wearing, and indoor contact restriction should be maintained to avoid a potentially disastrous impact on healthcare saturation.
Abstract
COVID-19 is a spectrum of clinical symptoms in humans caused by infection with SARS-CoV-2. The B.1.1.529 Omicron variant is rapidly emerging and has been designated a Variant of Concern (VOC). The variant is highly transmissible and partially or fully evades a spectrum of neutralising antibodies due to a high number of substitutions in the spike glycoprotein. A major question is the relative severity of disease caused by the Omicron variant compared with previous and currently circulating variants of SARS-CoV-2. To address this, a mouse model of infection that recapitulates severe disease in humans, K18-hACE2 mice, were infected with either a Pango B, Delta or Omicron variant of SARS-CoV-2 and their relative pathogenesis compared. In contrast to mice infected with Pango B and Delta variant viruses, those infected with the Omicron variant had less severe clinical signs (weight loss), showed recovery and had a lower virus load in both the lower and upper respiratory tract. This is also reflected by less extensive inflammatory processes in the lungs. Although T cell epitopes may be conserved, the antigenic diversity of Omicron from previous variants would suggest that a change in vaccine may be required to mitigate against the higher transmissibility and global disease burden. However, the lead time to develop such a response may be too late to mitigate the spread and effects of Omicron. These animal model data suggest the clinical consequences of infection with the Omicron variant may be less severe but the higher transmissibility could still place huge burden upon healthcare systems even if a lower proportion of infected patients are hospitalised.PS: The Neyts Lab at Leuven University in Belgium found that in Syrian hamsters, with a lower viral load in the lungs compared with other variants. But Prof Johan Neyts said this may be because the virus was better at infecting humans than hamsters, or that it was more likely to infect the upper respiratory tract, or that it provoked less-severe disease.
Also another study in the US using mice also shows similar results.
