This is quite technical and I’m not sure I understand it fully myself, but I’m going to have a go at trying to explain a point of disagreement between scientists arguing that cross-reactive T-cells have been responsible for protecting some people from Covid in the past and vaccine expert Geert Vanden Bossche who believes that there is no evidence for this phenomenon.
The Torygraph excitedly proclaims:
If you go to the article itself, written by Sarah Knapton, you read:
Large numbers of Britons were already protected from coronavirus before the pandemic began because of previous exposure to common colds, a groundbreaking new study suggests.
Researchers at Imperial College found that half of people living with an infected person in the second wave – before vaccines were available – were carrying high levels of memory T-cells from colds that may have stopped them picking up the virus.
First off, Knapton is pretty hopeless at identifying and citing her specific references. She confuses the reader by referring to two Imperial College studies, one published today (January 10th, 2022) and the other published much earlier, before the ‘vaccines’ rollout. She also throws in an unreferenced University College London study for good measure:
Early on in the pandemic, studies showed that some people carried immune cells that could recognise Covid-19 even though they had never been infected.
University College London even discovered that blood samples taken before the pandemic carried this immunity, but it was not known if it was actually stopping people picking up the virus.
To answer the question, Imperial recruited several hundred households in London last winter before the vaccine programme began, and took blood samples to measure levels of memory T-cells from colds before waiting to see who caught the virus.
Amidst this confusion of references and citations from various authors, we get to the real knub of the issue. It’s not that prior cross-reactive immunity meant that the populace was not equally susceptible to Covid infection – as claimed by Ferguson and the modellers at Imperial and as claimed by Whitty, Vallance etc. in defence of extreme control measures. It’s not that this incorrect assumption was used wrongly in the models to predict the occurrence of many more infections and deaths, thus justifying the initial, catastrophically harmful lockdown (and the two subsequent lockdowns). Oh no, that’s not even mentioned by Knapton. It’s all about developing new ‘vaccines’ on the basis of this ‘new, groundbreaking’ research:
Prof Lalvani added: “We’ve finally reached the Holy Grail which shows that those who were exposed but didn’t get infected had these types of T-cells. These are people who would have picked up a cold, one, two, three years before and their immune cells were in a memory state.
“Coronaviruses are a wide tribe, and these common cold viruses are quite far apart, yet even the T-cells targeting these distant relatives can cross-protect, so imagine if you took one of the core proteins of Sars-Cov-2 and put in a vaccine. The T-cells would cross-recognise variants which opens the door to a universal vaccine that will protect you against all current and future mutant strains as they arise.
“Such a vaccine would not need to be given as frequently because the memory T-cells last longer than the antibodies. We’re in this awful position where we need boosters every three months, but with T-cells you could cut it down to every year or two years.”
Pretty shabby ‘journalism’ from the Torygraph, as we’ve come to expect.
Geert Vanden Bossche is a bit of a hero in my opinion. Perhaps the most unlikely of heroes. A mild-mannered Belgian vaccine expert and former employee of the Bill and Melinda Gates Foundation. I do often wonder what happens when he comes across a phone booth!
He has warned from the word go about the dangers of mass vaccination with ‘leaky’ (non-sterilizing) vaccines and he has been almost universally ignored by the consensus ‘experts’. But he hasn’t given up and he keeps plugging actual science even if, at times, it’s a little hard for non-experts like myself to follow and interpret.
This is Geert’s advice for the unvaccinated:
The situation for the unvaccinated is now becoming increasingly difficult because of unjustifiable discrimination. However, I keep saying that the unvaccinated should now less and less worry about their health. Provided they were gradually increasing their contacts, their innate immune system should be well trained by now. Training will only pay off provided you’re in good health and you respect the rules (!) of a healthy lifestyle (which should be well known by now).
So, ‘yes’ even contacts with HEALTHY vaccinees should become less of a problem. It is critical though that people take their supplements (certainly vit C, Zinc) as soon as they don’t feel 100% fit. And keep taking your vitamin D during winter. Regular use of ginger and curcuma are a good idea too! Avoid large and frequent gatherings but make sure your immune system stays trained (so regular contacts are key!).
Last, but not least: mental health is critical, make sure you are in good company and do not fall victim of fear!
Can’t argue with that. Good man. He’s on our side, but more importantly he’s on the side of science and medical ethics.
When it comes down to actual science, he’s hard to beat, but also a little hard to understand at times! But this is what Geert has to say about the ‘hypothesis’ of cross-reactive immune T-cells:
I don’t know how many more contributions I need to write to kill this idea.
Quite recently I was once again confronted with a paper (L. Swadling et al. 2021; 1) leading some scientists to believe that pre-existing cross-reactive T cells against Coronavirus (CoV) replication-transcription complex (RTC) can abort infection and thereby prevent seroconversion against SARS-CoV-2 (SC-2).
The Swadling et al paper is yet another study, published November 2021, this time by University College London, which is not mentioned by Knapton, but is also on the subject of cross-reactive T-cells. The abstract says:
Here we hypothesize that pre-existing memory T cell responses, with cross-protective potential against SARS-CoV-2 (refs. 4,5,6,7,8,9,10,11), would expand in vivo to support rapid viral control, aborting infection.
It also says:
Our data highlight RTC-specific T cells as targets for vaccines against endemic and emerging Coronaviridae.
So it’s another ‘vaccine’ pushing study, which is not surprising, considering mass vaccination salesman, Professor Bollox himself, is listed as one of those involved:
So anyway, back to what GVDB says:
Firstly, the authors don’t even claim what many seem to infer from their publication—it merely suggests a role of these pre-existing RTC-specific T cells in aborting SC-2 infection (e.g., ‘we hypothesize that pre-existing memory T cell responses would expand to support rapid viral control, aborting infection’; ‘Pre-existing RTC-specific T cells would be expected to favor early control, explaining their enrichment after abortive compared to classical infection’ or: ‘suggesting abortive infection’, or: ‘supporting a potential role [of NSP12- specific T cells] in protection from PCR-detectable infection and seroconversion’). Secondly, I will illustrate below why this [peer-reviewed] paper does nothing to prove that pre-existing RTC-specific T cells with cross-reactive potential abort infection.
There is no single piece of evidence showing that natural CoV infection (or even any of the C-19 vaccines) induces Ag-specific cytolytic T memory cells. One is therefore unable to reasonably speculate that CoV-specific T memory cells prevent disease.
That seems fairly straightforward. So, here’s where it gets a bit more complicated and difficult to interpret what GVDB is actually saying:
Lack of consensus that immune protection against CoV (and likely against Flu as well) is primarily provided by self-centered innate immune effector lymphocytes (e.g., innate antibody [Ab]-secreting B cells and NK cells) and not by conventional foreign-centered T and B cells is only grist to the mill of those who advocate for C-19 vaccination across all age groups. So, not surprisingly, the authors of this article are proposing that ‘The boosting of such T cells may offer durable pan-Coronaviridae reactivity against endemic and emerging viruses, arguing for their inclusion and assessment as an adjunct to spike-specific antibodies in next-generation vaccines.’ On the other hand, however, they seem to realize that they may be missing the key mechanism that is responsible for abortion of SC-2 infection and that expansion of pre-existing RTC-specific T cells in seronegative (SN) health care workers (HCWs) is only the result of asymptomatic infection but not the cause: ‘A caveat of this work is that we analysed only peripheral immunity; it is plausible that mucosal-sequestered antibodies had a role in our seronegative cohort. It also remains possible that innate immunity mediates control in abortive infections, with RTC-biased T cell responses being generated as a biomarker of low-grade infection.’ And furthermore: ‘A transient/abortive infection that is not detectable by PCR or seroconversion could conceivably result from a lower viral inoculum and/or from a more efficient innate and/or adaptive immune response.’
Here’s what I think GVDB is saying:
/ Protection from SARS-CoV-2 can be achieved via the innate immune system, which is our first line of defence against pathogens, and includes the mucosal immune system which I previously wrote about. With respect to an airborne respiratory virus, the defensive role played by the mucosal immune system consisting of the mucus membranes inside the nose and throat is obviously very important. We’ll come back to this. The authors confirm that the mucosal innate immune system may be playing a part in preventing infection when they say: A caveat of this work is that we analysed only peripheral immunity; it is plausible that mucosal-sequestered antibodies had a role in our seronegative cohort.
/ Immune protection from cross-reactive adaptive B and T-cells is not the primary reason why immune naive (i.e. those not previously exposed) people don’t get infected with SARS-2. Indeed, the existence of this immune response is not evidence of prior cross-reactive immunity, it is evidence of prior infection with SARS-2. The authors confirm this as a possibility when they say: It also remains possible that innate immunity mediates control in abortive infections, with RTC-biased T cell responses being generated as a biomarker of low-grade infection.
/GVDB points out quite rightly that the study is being used as a platform for the development of next generation ‘vaccines’ across all age groups. On this aspect he is particularly scathing:
It’s also difficult to understand why the authors of this and similar SC-2 T cell-dedicated papers are not more skeptical about their own conclusions or postulates on using conserved, cross-reactive T cell epitopes in future C-19 vaccines. Are they unaware that there are no licensed or ‘successful’ candidate vaccines that (universally!) induce T cell-based abrogation of infectious transmission? Or that no vaccines exist that use non-structural proteins as targets for fighting infectious pathogens? All fields in infectious diseases, whether dealing with viruses, bacteria, or parasites, have explored T cell-based immune interventions to abrogate infection and prevent or cure disease, but all have miserably failed. In contrast to what the authors state, T cells don’t seem to be particularly effective vaccine targets.
In conclusion, GVDB dismisses T-cells as being functionally important in preventing infection in immune naive or previously exposed individuals or terminating infection in such individuals:
SC-2 reactive T memory cells are neither responsible for early nor for late abrogation of SC-2 infection and, therefore, can neither prevent nor terminate C-19 disease.
So this is where it gets interesting because it appears that something did indeed prevent many people early on in the pandemic from getting infected with SARS-CoV-2 or suffering moderate to severe symptoms. If it wasn’t cross-reactive T-cells from prior infection with the common cold viruses, what was it? Maybe this study gives us a clue:
Interestingly, circulating SARS-CoV-2–reactive T cells have been described in SARS-CoV-2 naive individuals, and it has been suggested that they may have arisen from encounters with related coronaviruses (6–10).
The authors acknowledge the common cold cross-reactive T-cell hypothesis. But here’s what they find:
Epidemiological studies indicate that asymptomatic infections or infections with a mild course of disease can frequently represent the majority of the study population (15). These observations suggest that the mucosal immune system of the upper respiratory tract may play a role in limiting disease severity in a significant percentage of SARS-CoV-2 infections. This prompted us to explore the presence of mucosal SARS-CoV-2–reactive B cells in tonsillar tissue specimens collected from pediatric patients 3 or more years prior to the outbreak of the Covid-19 pandemic.
In this study, we report the identification of pre-existing mucosal SARS-CoV-2–reactive Abs. These Abs are encoded by naive and Ag-experienced B cells, exhibit neutralizing potential, and do not recognize endemic human coronaviruses.
This is quite an extraordinary finding. They identify SC-2 reactive mucosal B-cells in children from before the pandemic, but these same cells are not reactive to the common cold viruses, so it’s not a case of cross-reactivity via exposure to other common coronaviruses.
Recent studies showing S-protein reactivity of sera collected from SARS-CoV-2–negative individuals suggest that a previous encounter with endemic HCoV may be a potential source of pre-existing circulating S-protein–reactive Abs (11, 13).
We observed that our panel of Abs readily recognized the wild-type SARS-CoV-2 S-proteins with a small subset of Abs also binding to the S-protein of SARS-CoV but that none of the Abs showed reactivity to the S-proteins of the endemic HCoV-OC43 and HCoV-229E coronaviruses (Fig. 3D, 3E).
The authors clearly identify a role for the innate mucosal immune system in the prevention of infection from SARS-CoV-2, which has nothing to do with cross-reactive T-cells.
Our detection of pre-existing SARS-CoV-2–reactive Abs in the mucosal immune system of the upper respiratory tract that, although lacking the potency of neutralizing Abs isolated from Covid-19 convalescent individuals, exhibit the ability to partially block ACE2 binding in vitro provides an as-yet-unexplored contribution of the mucosal adaptive immune system to pathogen protection.
Prepandemic serum samples were reported to cross react to SARS-CoV-2, indicating that humoral immune responses to endemic HCoV may engage the viral pathogen following infection but they do not correlate with protection from SARS-CoV-2 (11, 13). In our analysis, we did not observe cross-reactivity of the mAbs with the endemic HCoV-OC43 and HCoV-229E
Humoral immune responses are those which occur in the blood and the lymphatic fluid, as distinct from mucosal. The authors here identify prepandemic mucosal neutralising antibodies which have played a role in preventing people from getting infected with, or seriously suffering from SARS-CoV-2, which are not related to previous exposure to the common cold. The origin of this pre-existing immunity is therefore a bit of a mystery, but it does explain why children in particular are less susceptible to infection with SARS-CoV-2.
We are left to contemplate how important T-cells actually are in preventing infection and serious disease from Covid versus the importance of mucosal immunity mediated via immune cells in the upper respiratory tract. We are also left to contemplate what role each played in the protection of the populace from the newly emergent SARS-CoV-2 virus very early on in the pandemic and how that prior immunity actually arose, if it was not from exposure to the common cold.
It would appear that the Imperial College London study was started in September 2020 but has only just now been published. This is a ridiculously long time to take to publish data which was collected over a year ago.
It’s good to have further confirmation of this from Imperial (and also recently from UCL), but it has to be said it’s pretty late to the party, and it’s not clear why a study which began in September 2020 during a public health emergency has taken 16 months to report, particularly when vaccines were brought to market in 10 months.