Does SARS-CoV-2 infection result in immune damage or a syndrome comparable with AIDS?
No, of course not.
This is an attention-seeking post from an organization calling itself the World Health Network (WHN). Despite the name, this is not an official body like the World Health Organization (WHO), though they attempt to project a similar public service role. However, it's important to clarify that WHN does not serve the same function and has no official capacity.
The group describes itself as "a global community devoted to protecting health and minimizing harm to individuals and society in the face of the COVID-19 pandemic." Their team, a diverse collection of individuals, can be found here: Meet Our Team. Notably, the members come from a wide range of backgrounds, including nursing, film, engineering, chemistry, and epidemiology. However, it’s striking that none of them have expertise in biology, particularly in virology and immunology—fields critical to their mission, which focuses specifically on the SARS-CoV-2 virus, the COVID-19 disease, and the immune response.
This lack of relevant expertise has led to numerous incorrect statements, flawed conclusions, and misinterpretations of scientific literature, often presented without the necessary context. Currently, they are spreading a deeply concerning and incorrect message, claiming that SARS-CoV-2 infection results in "AIDS-like features." This claim not only contradicts their stated goal of "promoting safety and support for everyone" but also spreads misinformation that can cause unnecessary fear and confusion.
AIDS, or acquired immune deficiency syndrome, is a devastating disease first identified in the 1980s. Unfortunately, it remains a global health issue, with people continuing to be infected by its causative agent, the human immunodeficiency virus (HIV). HIV is a retrovirus that, once it enters the body, integrates into the host's genome. It can remain dormant for years, only to be reactivated at any time. HIV primarily targets a subset of immune cells known as T lymphocytes, or T cells. These are crucial for coordinating the body's immune response. T cells are divided into two main types: CD8 T cells, which can directly kill infected cells, and CD4 T cells, which are the main target of HIV. CD4 T cells play a critical role in regulating and enhancing the functions of other immune cells, including CD8 T cells and antibody-producing B cells.
As HIV infects and kills CD4 T cells, their numbers gradually decline. Once they fall below a critical threshold, the immune system becomes severely compromised. At this point, the body struggles to fend off pathogens that would typically be easily managed. These opportunistic infections can cause serious harm and, eventually, lead to death as the body's remaining defenses are overwhelmed. AIDS is a truly devastating disease, not only because of its physical impact but also due to the stigma that surrounds it. Fortunately, we now have highly effective medications that can control the virus, allowing those affected to live largely normal lives. However, this requires daily adherence to a regimen of anti-retroviral drugs.
Now enter the mindset of the WHN members to claim that the coronavirus, a respiratory pathogen, causes an AIDS-like syndrome. This is an extraordinary claim, and will need to be substantiated by extraordinary evidence.
Why extraordinary? We know about coronaviruses, how they infect, how we mount an immune response. Sure, there are still details to be discovered, things that are not exactly the same as the other coronaviruses, OC43, NL63, HKU.1 and 229E that frequently infect us. SARS-CoV-2 is relatively new still and has caused a lot of damage. But, it is not a retro-virus, it does not integrate in our genome, it does not compromise our immune system. However, lets look at the claims made.
The statement begins strongly: people do get infected, in waves. While numbers aren't the focus here, it's important to recognise that SARS-CoV-2 can cause damage. The key word is "can." Any pathogen has the potential to cause harm to various tissues, but that doesn’t mean it always will. Our immune system plays a crucial role in preventing this damage. SARS-CoV-2 caused significant harm early in the pandemic because our immune system encountered it for the first time. While many people successfully cleared the virus, our acquired immune defenses were unprepared. Over time, however, our immune system—thanks to vaccination and prior infections—has developed powerful defenses, including T cells and antibody-producing B cells. For most of us, this means that an infection is now swiftly controlled (which may still involve symptoms).
Unfortunately, this won’t be the case for everyone. The capability and strength of the immune system decline with age, or may be compromised by disease or medication. This is an important point to understand: biology isn’t a matter of 0% or 100%—we’re dealing with a range of outcomes.
SARS-CoV-2, like the NL63 coronavirus, binds to ACE2 receptors, which are expressed on many cells, including those in the lungs and blood vessels. Despite this, SARS-CoV-2 primarily causes respiratory disease, infecting the upper airways where the immune system typically controls it. In some cases, the virus may spread further to the lungs and cause more severe disease. In rare cases, it can disseminate to other organs. This pattern is similar to most infections; for example, influenza often targets the lungs more than the upper respiratory tract and can disseminate if not controlled https://febs.onlinelibrary.wiley.com/doi/10.1111/febs.16363.
The WHN is spreading the message that extreme outcomes are the norm. To support their argument, they cite a paper titled "COVID-19: a complex multisystem disorder" from the British Journal of Anaesthesia. However, it’s important to note several things about this reference:
The British Journal of Anaesthesia is not a leading journal for virology or immunology.
The paper was published in 2020, at the very start of the pandemic when immunity was virtually nonexistent, leading to more severe illness as the virus could spread more easily. This does not reflect the current situation.
The paper is a review that summarises observations in patients who were so severely ill they required hospital care. It was intended to inform anaesthetists and intensive care specialists—not to provide a general overview of SARS-CoV-2 infections for the public.
A particularly frightening scenario would be SARS-CoV-2 infecting the brain. However, this is extremely unlikely. Neurons are not easily infected by SARS-CoV-2, even in laboratory settings where the virus is present in high concentrations. That said, while rare, it’s not impossible for the virus to reach the brain in some cases. The reference provided for this concern is a study published in Nature: SARS-CoV-2 in the Brain. But does this study really apply to "the million people infected with SARS-CoV-2 each day"?
The study examined autopsies of 44 patients who died with COVID-19, and brain samples from 11 of them. These cases represent extreme outcomes, not the norm.
The study detected viral RNA, not the actual virus, and found no evidence of cells being damaged by the virus or of local immune responses. This suggests the presence of viral remnants, not infectious virus.
The autopsies were conducted between April 26, 2020, and March 2, 2021—during the early waves of the pandemic, before vaccines were available.
The median age of the patients was 62.5 years.
This study reflects a specific period in the pandemic, when immunity was virtually nonexistent, and it focused on individuals who were older and more vulnerable—people who, tragically, succumbed to the infection. It shows what can happen under particular circumstances, not what is typical or likely for most people today.
The claim that SARS-CoV-2 causes premature aging is another point raised by the WHN. To support this, they reference their own publication (Joffe, D., Bilodeau, S., Šalamon, Š., Ewing, A., Bar-Yam, Y., Pretorius, R., & Fox, G. Spectrum of COVID-19: From Asymptomatic Organ Damage to Long COVID Syndrome. WHN Communications, 2024, 5(3)), presenting it as if it were a scholarly work. However, this paper suffers from many of the same issues we've already discussed, and I will not delve into it further.
They also cite a study published by MDPI, a journal known for its minimal peer review and frequent publication of substandard work: MDPI Paper on Telomeres. The study supposedly demonstrates aging by pointing to the shortening of telomeres, the protective caps at the ends of chromosomes, in patients with long-term symptoms of COVID-19 (commonly referred to as Long COVID). These patients were compared to individuals who had never been infected. During a severe infection, tissue damage occurs, followed by repair, which involves cell division and consequently, telomere shortening. However, telomeres can be lengthened again, so this is not necessarily a permanent change. The study does not provide information on when the samples were taken post-infection, leaving open questions about the context of these findings. Were the patients with severe COVID-19 already at higher risk because they had shorter telomeres to begin with? This seems likely, as shorter telomeres are indeed a known risk factor, and the WHN appears to have confused cause and effect Accelerated biological aging in COVID-19 patients.
Lastly, the WHN refers to another study, published in Nature, which claims that SARS-CoV-2 can infect T cells: Nature Paper on T Cells. However, the data presented is not convincing. The proportions of infected T cells are extremely small, even in laboratory conditions, the microscopy staining is inadequate, and there is no clear mechanism for how the virus enters these cells, as ACE2 and TMPRSS2—known entry points for the virus—are not required. Moreover, if the virus does manage to enter T cells, it doesn’t seem to lead to a productive infection. In contrast, there is substantial high-quality evidence showing that SARS-CoV-2 infections result in robust T and B cell responses, which are critical in controlling subsequent infections. The virus-specific T cells generated in response to infection are highly effective, as demonstrated in numerous studies T Cell Responses to SARS-CoV-2 | Annual Reviews.
The WHN continues with more claims about the effects of SARS-CoV-2 on the brain. While it's true that infections can accelerate pre-existing conditions and cause temporary changes in brain structure, this is not unique to SARS-CoV-2. These points seem to be included primarily to instill fear and anxiety, which is in stark contrast to their stated goal of "promoting safety and support for everyone."
Similarly, they emphasise the potential for long-term issues, a phenomenon that can occur with any infection. As shown in Table 2 from this study, post-acute infection syndromes have been documented following various viral and non-viral infections. These long-term effects were more pronounced early in the pandemic, largely due to the absence of immunity.
Given these broader concerns, I will now turn my attention to addressing the WHN's alarming and misleading claims about AIDS.
Contrary to the WHN's claims, there is no broad consensus among scientists warning about these issues. The alarm is primarily being raised by members of the WHN and a few social media accounts, not by experts in immunology or virology. In fact, none of the references they cite support their claims.
Reference 13 does not support the idea that SARS-CoV-2 causes AIDS.
Reference 14 is a poorly conducted in silico study, which lacks empirical validation https://x.com/Marc_Veld/status/1821201983761535067.
Reference 15 discusses epigenetic changes related to inflammation in the context of "innate immune cell training," but it certainly does not claim that SARS-CoV-2 causes AIDS.
The WHN then tries to pivot by claiming that while SARS-CoV-2 might not cause AIDS, it has deleterious effects on the immune system. However, they cherry-pick studies to support this narrative, ignoring the substantial body of research showing that SARS-CoV-2 infections typically result in robust immune responses and long-lasting immune memory. This is why recent waves of SARS-CoV-2 have been characterised by relatively mild illness and the absence of a large-scale health crisis.
The WHN's references further undermine their credibility:
Reference 16 is actually a news story, not a scientific study. The scientific reference they likely intended to cite is actually Reference 15. It's unclear whether the authors mistakenly duplicated this reference or did so intentionally.
Reference 17 is a review article published in Frontiers, which presents no primary data. The review is highly speculative, mainly drawing parallels between CD4 T cells in HIV and those in acute-phase severe COVID-19 patients from 2020—comparisons that are not well-supported by accurate data.
Reference 18 comes from a less reputable journal and is essentially someone’s opinion, not backed by solid scientific evidence.
Reference 19 is a preprint from July 2020 that has not undergone peer review. Citing such an outdated and unreviewed study suggests they are scraping the bottom of the barrel for support.
Reference 20 is another Frontiers article, this time comparing immune and metabolic responses. However, it makes no claims about SARS-CoV-2 causing any “AIDS-like” conditions.
Reference 21 no references to AIDS or immune damage.
It seems that the WHN members simply Googled "AIDS and COVID-19" and compiled whatever they found, regardless of quality or relevance. This approach does not build a convincing or scientifically sound argument.
The WHN also attempts to link COVID-19 to cancer, but their references are again questionable:
Reference 22 is their own blog post, which is not a scientific source and lacks credibility.
Reference 23 does not even address COVID-19; it focuses on primary immune deficiency patients, which is unrelated to their claim.
Reference 24 discusses the possibility that increased susceptibility to SARS-CoV-2 could be due to an already existing cancer, not the other way around.
Reference 25 is simply an opinion piece, offering no solid evidence.
Reference 26 and 27 is another opinion article speculating that viral infections like SARS-CoV-2 might increase the risk of cancer. However, it does not argue that SARS-CoV-2 causes AIDS-like symptoms or that these symptoms lead to reduced cancer surveillance.
The WHN's citations here are misleading, presenting speculative arguments and opinions as if they were established facts. This approach does not support their alarming claims about the relationship between COVID-19 and cancer.
The WHN's argument suggesting that SARS-CoV-2 could cause immunodeficiency similar to how HIV leads to AIDS 10-15 years after infection is alarmist and unfounded. SARS-CoV-2 does not cause long-term damage to the immune system, and such claims amount to scaremongering. The idea that "immunodeficiency" develops weeks or months after SARS-CoV-2 infection is not supported by evidence. T cells are functioning effectively, and there is no indication of immune exhaustion from SARS-CoV-2.
Examining the references they provide:
Reference 30 is a study published in Frontiers in May 2020, which only includes severe COVID-19 cases. The results are specific to ICU patients, who often experience lymphopenia due to various factors. Persistent lymphopenia is a risk factor for ICU-acquired infections and for death in ICU patients with sustained hypotension at admission | Annals of Intensive Care | Full Text (springeropen.com).
Reference 31 discusses a common viral strategy to evade immune detection by interfering with antigen presentation, such as reducing MHC I expression. This is a tactic for immune evasion, not evidence of immune dysfunction or AIDS.
Reference 32 examines CD19 expression on B cells. While it notes reduced CD19 expression, this is not indicative of immunodeficiency and has not been consistently observed across other studies. Functional consequences of this finding are not established.
Reference 33 addresses epigenetic dysregulation following an immune response, but it does not provide evidence of immune system damage or immunodeficiency. It also lacks infection controls, which limits its relevance to the broader context of SARS-CoV-2's impact on immunity.
Reference 34 is another WHN blog post, which, like their other blog entries, lacks scientific rigor.
Reference 35 I know the authors will not agree with the WHN interpretation. More explanation here; https://x.com/Marc_Veld/status/1617562429919051776 And subsequent 24 month follow up showing how it improves here; https://x.com/Marc_Veld/status/1780856204522135933
The WHN’s claims about SARS-CoV-2 causing AIDS-like immune dysfunction are not supported by credible evidence and reflect a pattern of misrepresenting or misinterpreting scientific findings to promote fear.
The WHN members have made a series of unsubstantiated points that need clarification:
· Repeat Infections and Dysregulation: There is no evidence to suggest that repeat infections with SARS-CoV-2 lead to immune system dysregulation or damage.
· Long COVID and AIDS-like Symptoms: Long COVID is a serious condition, but it does not cause "AIDS-like" symptoms. It presents its own challenges, but these are not comparable to the immune system destruction seen in AIDS.
· Immune Response to Pathogen Reencounter: Reencountering a pathogen, including SARS-CoV-2, stimulates the immune system. This re-stimulation boosts the number of immune cells, replenishes antibody levels, and broadens the immune response. This is a normal immune function and enhances your defense against future variants. While infection is not ideal, it helps strengthen the immune response.
· Understanding of Herd Immunity: The WHN appears to misunderstand herd or group immunity. Their team lacks expertise in immunology, as noted in critiques Marc Veld's Tweet.
· SARS-CoV-2 Surveillance: SARS-CoV-2 is actively monitored through wastewater sampling, sequencing, and the annual update of vaccines. The risk posed by SARS-CoV-2 is now comparable to other common infections like influenza and RSV.
· Virus Evolution: SARS-CoV-2, like all viruses, continues to evolve and mutate. This is a natural process and not unique to SARS-CoV-2. It should not be used to create unnecessary fear.
· Infection Frequency and Symptoms: Regular infections with viruses such as influenza, rhinoviruses, adenoviruses, and RSV are common. Typically, you might encounter these viruses every 2-3 years. Symptoms usually result from your immune system responding to the virus. Using emotive arguments, such as those involving children, does not contribute to a scientific understanding of the situation.
The WHN’s claims are based on misunderstandings and a lack of scientific evidence. Their attempts to link SARS-CoV-2 to severe immune dysfunction and other issues are not supported by credible data and reflect a broader pattern of misinformation.
The WHN’s views are marked by unrealistic expectations and misunderstandings:
Eliminating SARS-CoV-2: It is highly unlikely that we will be able to eliminate SARS-CoV-2 entirely. The virus is highly infectious and has large animal reservoirs, making eradication impractical.
Use of Masks and Respirators: While masks and respirators can be beneficial for individuals who choose to use them or are advised to do so, they are no longer recommended for universal use. Public health guidelines have shifted based on the current understanding of the virus and its transmission.
Clean Air and Respiratory Infections: Maintaining clean air is beneficial and can help reduce some respiratory infections. However, it is important to recognise that respiratory infections will still occur despite efforts to improve air quality.
The WHN appears to struggle with accurately interpreting scientific literature and relies on fear-based tactics. Their approach reflects a broader trend of using scare tactics about a disease to generate fear and concern about SARS-CoV-2, despite the reality of the data showing otherwise. They seem more focused on amplifying fear than on providing balanced, evidence-based information.
In conclusion, the WHN’s claims about SARS-CoV-2 and its supposed “AIDS-like” effects, cancer risks, and other exaggerated dangers are not supported by credible scientific evidence. Their approach, marked by fear-mongering and misinterpretation of data, undermines public understanding and can contribute to unnecessary anxiety. The reality is that while SARS-CoV-2 remains a concern, current data and expert consensus highlight its manageable risk and the effectiveness of our immune responses. It's crucial to rely on accurate, evidence-based information from experts and not be swayed by alarmist rhetoric.
'A particularly frightening scenario would be SARS-CoV-2 infecting the brain. However, this is extremely unlikely. Neurons are not easily infected by SARS-CoV-2, even in laboratory settings where the virus is present in high concentrations.' Several reports show otherwise.