A global team of experts headed by scientists Yaneer Bam-Yam and Andrew G. Ewing revisited the long-term consequences of COVID-19 with renewed urgency as emerging evidence suggests the virus may trigger persistent immune disruptions in some individuals. A growing debate has surfaced over whether comparisons to AIDS, once dismissed as alarmist, might reflect deeper biological and public health concerns.
Airborne Transmission and Lasting Immunologic Impact: Reassessing COVID-19 Through a Comparative Lens
Provocative Phrase Gains Public Attention
The expression “Airborne AIDS” emerged from advocacy groups and select scientists who saw troubling signs of persistent immune changes.
Public concern over viral persistence and post-infection illness grew as physicians documented lingering symptoms in patients long after initial recovery from SARS-CoV-2. Reports of chronic fatigue, neurological impairment, and immune irregularities prompted researchers to revisit earlier assumptions that COVID-19 was strictly an acute respiratory disease.
The term “Airborne AIDS” began circulating in select scientific and patient advocacy circles as evidence of immune disruption accumulated. It drew attention because it linked a transmitted respiratory virus with a stigmatized immunodeficiency condition. This has forced comparisons that most experts originally viewed as an exaggeration and unsupported.
Advances in diagnostic methods revealed traces of viral material in tissues months after infection in some individuals. Studies reported indicators of chronic inflammation, irregular T cell behavior, and potential organ involvement. These findings created a foundation for researchers to investigate whether SARS-CoV-2 could generate long-term immune consequences.
Understanding SARS-CoV-2 Further
Signs of immune disruption that persisted well beyond acute infection were discovered and have prompted deeper investigation into the virus.
The team of Bam-Yam and Ewing wrote a comparative narrative that reviewed and compared all available data about immune dysfunction and systemic sequelae following SARS-CoV-2 infection with similar features seen in HIV infection. They wanted to know whether the analogy that COVID-19 is airborne AIDS is a useful provocation for science and policy.
Note that studies on SARS-CoV-2 have extended beyond respiratory complications. Observations of persistent physiological changes prompted closer inspection of how this coronavirus interacts with immune pathways, inflammatory mechanisms, and cellular recovery processes that normally return to baseline following most common viral infections in humans.
Reports showed reductions in lymphocyte populations, irregular T cell responses, and lingering inflammatory markers in subsets of patients. These findings suggested that the virus might induce immune exhaustion resembling patterns seen in chronic infections. The extent and duration of this condition appeared variable across demographics and clinical histories.
The phrase “Airborne AIDS” did not originate within large institutions but rather circulated among patient advocates and smaller research groups alarmed by emerging trends. Early adopters used the term to draw further attention to chronic outcomes that seemed underreported or minimized in both mainstream public health messaging and mainstream media reporting.
Some clinicians described the language as exaggerated. But the terminology persisted because it framed a broader concern about post-infection vulnerability. Discussions spread through various digital forums, conference presentations, and media interviews, where supporters argued that metaphors could stimulate faster policy responses and research investment.
Additional studies discovered remnants of SARS-CoV-2 persisting in tissues and organs months after initial COVID-19 illness. Tissue samples from gastrointestinal sites, lymph nodes, and neurological regions showed evidence of lingering viral material that could sustain immune activation. This is somewhat similar to HIV reservoirs in HIV infection cases.
The similarities between neurological syndromes due to long COVID or SARS-CoV-2-associated neurological disorders and HIV-associated neurocognitive disorder have also been drawn. These include brain lesions due to inflammation, various cognitive issues due to cognitive impairment and neurological decline, and overlapping clusters of symptoms, among others.
Biology that Shapes Public Understanding
The two viruses and resulting diseases behave differently at molecular, clinical, and population levels despite overlapping immune disruption outcomes.
Note that the researchers have underscored the fact that they were not arguing that SARS-CoV-2 and HIV are the same. They are highlighting the need to examine the overlapping downstream phenomena caused by these two viruses. The narrative review was intended to promote an analogy that will provide a provocative lens for thinking about public health preparedness.
SARS-CoV-2 and HIV differ significantly in biological structure and replication behavior. It is worth mentioning that HIV is a retrovirus that integrates into host DNA and directly targets CD4 lymphocytes. SARS-CoV-2 is a coronavirus that primarily infects respiratory and epithelial cells without permanent genomic integration or identical immune cell depletion.
The researchers still note that SARS-CoV-2 can cause immune deficiency. Calling COVID-19 airborne AIDS emphasizes the fact that the causative virus spreads via respiratory transmission rather than sexual contact, and the potential scale of immunity-related disorders may exceed models previously associated with localized or behavior-linked pathogens.
FURTHER READINGS AND REFERENCES
- Salamon, S., Kruger, A., Lupton, D., Pretorius, E., Ewing, A. G., and Bar-Yam, Y. 2025. “COVID-19 is ‘Airborne AIDS’: Provocative Oversimplification, Emerging Science, or Something in Between?” AJPM Focus. 100458. DOI: 1016/j.focus.2025.100458