bhobba said:
I agree it is unrealistic to stop community transmission entirely. You only have to look at the Sydney outbreak. It is made worse by population pockets with high numbers of immigrants. To many of them, limiting contact to family members in the same household also means their extended family in different physical households. It is cultural. The same thing happened with the Melbourne outbreak. Some communities were not getting the message for cultural reasons. A good friend of mine when young moved from Canberra to Perth, where his family was. He was second generation Australian. When I visited for a few weeks to watch America's Cup, I was shocked at just, culturally, how different his parents were to their sons and daughters. They had to still explain many things to them, and their English was poor. They even had to ask me about things.
The current vaccines are good, but the rate variants keep popping up, new vaccine development is needed. We also would like to eliminate the minimal risk they have of thrombosis, heart issues etc.
But we need to be careful. We tinkered with the Whooping Cough vaccine to reduce rare side effects. That worked, but it is now not as effective, meaning here in Aus, we have this no jab no pay rule. If no vaccination against Whooping Cough, then no government supplements, tax concessions, or even enrolling in a government school.
Thanks
Bill
Actually, you have just reminded me of a very important effect of vaccination with the mention of Whooping cough. The original vaccine was produced using killed cells of the whole pertussis bacterium. While this process introduced a very wide range of antigens some of which induced adverse reactions it was decided to produce a vaccine from selected 1–5 purified pertussis proteins, this was shown to be just as immunogenic while causing fewer problems. The preliminary clinical trials in the 1990s comparing the two suggested comparable efficacy and immunogenicity.
However, more recent data have shown that the disease is not adequately controlled and outbreaks have occurred, even in countries with extensive vaccine coverage. The higher antigenic load of the whole cell vaccine may explain the epidemiological evidence that supports the longer lasting protection induced by these vaccines, the purified protein vaccines may also lack some potentially protective antigens in the whole cell formulations.
There is now evidence that
B. pertussis and
B. parapertussis have adapted to the restricted niches of hosts, in highly vaccinated populations. It seems that circulating strains of
B. pertussis are evolving to evade the vaccine-conferred immunity, in this it is the vaccine itself which acts as the selective force.
So far I haven't seen any comments that explicitly address the effects of the vaccination program, and there is a continuing debate as to the relevance of the new variants. It is for example suggested that the delta variant is more infectious / transmissible, and this reflects some new quality of the virus. In fact, the delta variant has become much more widespread as the vaccination program has been developing, and this virus has shown itself to be resistant to the effects of at least 1 monoclonal antibodies, an antibody that all the current vaccines stimulate. Evolutionary theory suggests that over time, a relatively small selective advantage can have a massive effect on the overall population.
As the delta variant finds it easier to become established in populations with relatively low levels
of immunity, that's all that is needed to provide the selective advantage over the current strain in rates of infection. However, this variant has no additional tools to counter the T cell response induced by all the current vaccines, so it still runs a course that is time limited and therefore milder.
This would suggest that the delta variant has no adaptations that make it more transmissible or deadly, what we are seeing is a fitness advantage because of changes in the host population, induced by vaccination. In non-immune populations, it would still predominate if this was the first variant the population was exposed to, it is likely to have all the abilities of the first variant, which wasn't of course the original variant identified in people.
When we talk about the evolution of changes in the way an organism interacts with its environment the first consideration should be issues of fitness, we tend to apply our own human biases to explanations of changes. We tend to think of the changes in the number of infections as synonymous with increased virulence, so we see the increase in the delta variant as more dangerous. In fact we can only get an estimate by comparing the spread of two variants in a non-immune population, so really we don't know. While it has become more common in immune or partially immune populations, in terms of the numbers of associated deaths, it seems to have made little if any difference. For a virus, causing serious disease or death actually limits its fitness and evolution if nothing else almost guarantees things will change. The most successful pathogens tend to be associated with a long period in which they can infect others, be asymptomatic or at least have mild symptom's so that the victim maintains social contacts, can avoid at least some of the bodies defences and if it does kill someone it takes a long time to do it. SARS had a very short incubation period, during which it couldn't spread, it caused profound illness, people automatically isolated themselves and rapidly lead to the deaths of many it infected. It no longer infects anyone, the virus is, in effect, extinct.
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