As we learned yesterday evening, a new and more infectious Covid strain, named VUI-202012/01 or B.1.1.7, recently emerged in London and southeast England theguardian.com/world/2020/... With crowds fleeing the capital last night, before a travel ban came into effect, it seems almost certain that the new strain will take root elsewhere.
Concerns about the new strain are:
- its potential to turbocharge the spread of the virus, infect greater numbers and overwhelm the health service - at the moment this is a distinct possibility
- its potential to make people more severely ill - at the moment there is no evidence for this
- its potential to make vaccines less effective - at the moment there is no evidence for this.
So who are the scientists tasked with analysing coronavirus mutations and their effects on the course of the pandemic? In the UK it's the Covid-19 Genomics UK Consortium (COG-UK), whose preliminary assessment of variant B.1.1.7 says:
"This variant has 17 mutations (the 14 amino acid replacements and 3 in-frame deletions are listed in Table 1b). Two of these mutations have already been described to alter SARS-CoV-2 biology: N501Y sits in the receptor binding motif (RBM) of the Spike protein, and has been described to increase binding affinity to the human ACE-2 receptor; 69-70del has been identified in variants associated with immune escape in immunocompromised patients and is responsible for a “dropout” in the S gene PCR target in certain diagnostic tests (e.g. Thermo Fisher TaqPath). These tests target multiple regions of the virus genome, so the test itself is not compromised. Reported cases and phylogenetic analyses have indicated an exceptional rate of introduction of mutations into this lineage. It has been hypothesised that this lineage may have resulted from the transmission of the virus from a chronically-infected individual. This is based on observations that a high rate of mutations may accumulate In immunocompromised patients with chronic infections of SARS-COV-2" cogconsortium.uk/wp-content...
This is highly complex technical data with concerning implications for the immunocompromised (though to what extent is yet undetermined). I found this explanation much simpler to digest at this point but would still appreciate the insight of any molecular/epidemiology/ virology scientists etc. amongst us.
The BBC article is a good summary of what's going on. Although the COG-UK update is technical, what stood out for me was "observations that a high rate of mutations may accumulate in immunocompromised patients with chronic infections of SARS-COV-2". This ties in with accounts of immunosuppressed Covid patients, showing protracted infection with viral shedding over many weeks nejm.org/doi/full/10.1056/N... and cell.com/cell/pdf/S0092-867... The latter is a case study of a CLL patient who was shedding potentially infectious virus for the better part of 10 weeks. Interestingly, the patient was essentially asymptomatic, giving weak antibody titres despite receiving convalescent plasma, with the virus mutating continuously.
So what does this all mean for immunosuppresssed CLL patients? As for everyone, if Covid is becoming more infectious we may need to take even more care not to catch it. But if we do catch it, our symptoms may look very different from the norm; and in the worst case we may not recognise we have Covid, while remaining infectious over a period of many weeks.
Can anybody explain how asymptomatic patients can shed or spread the virus? Does it have to be some coughing or sneezing to make those air droplets containing the virus? Thanks.
Simple! Just breathing can expel the virus. Talking, particularly if loudly, or even more shouting or singing greatly increases the amount of shedding. That's no doubt one of the reasons pubs/bars are often included in restrictions.
I'm sure AussieNeil can answer your question better, but simplistically... the body sheds virus in ways other than in coughs and sneezes. Virus particles anywhere in the respiratory tract can simply be breathed out, while particles in the digestive tract will be excreted. Whether symptomatic or not. Shed particles may be dead or incapable of replication, as typically in later stages of infection. But at earlier stages, including pre-symptoms, the infected individual may shed enough viable particles into the environment to transmit the infection to someone else. The finding that some immunocompromised individuals can remain asymptomatic while shedding viable virus particles over a period of weeks or months is disturbing.
I cannot help feeling that the evolution of the virus was always going to happen. From memory of a presentation back in May I think the good news was that it does not mutate as fast as the flu virus so hopefully the vaccine will be more durable in terms of how long it will be effective before tweaking is needed.
On a separate point from the original post, I was horrified at the crowds on platforms ‘fleeing London’ the other night - at best acting as a catalyst for the rest of the UK.
best to all, please stay safe, we will get through with some thought, rob
I have read that there are new strains or strain of COVID in the US and in Great Britain, and am now wondering if that means the current vaccines that just came on the market won't work for the new strains????
I still think trying to keep your immune system as strong as possible is the best defense against the virus, or any infectious disease. And the recovery rate for most people with good immune systems and under 65 is still 99.5% or greater according to the CDC.
Yes of course, but that is of limited help to those of us whose immune system has been destroyed by CLL plus chemoimmunotherapy. Our best defences are scrupulous hygiene and physical separation from society.
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Covid Vaccine for Immunocompromised 
Vaccine candidate was found to be more than 90% effective in preventing COVID-19 in participants without evidence of prior SARS-CoV-2 infect
COVID-19 among fit patients with CLL treated with venetoclax-based combinations
