Vaccines, infections and chronic diseases: A new understanding

Vaccines, infections and chronic diseases: A new understanding

The long-standing division between infectious (communicable) and non-communicable (chronic) diseases is collapsing under the weight of new epidemiological evidence. Mounting data reveal that viral pathogens are not transient threats but durable drivers of chronic conditions—chief among them, cardiovascular disease (CVD).

This reorientation is underscored by a comprehensive systematic review and meta-analysis led by Dr. Kosuke Kawai and colleagues at the University of California, Los Angeles, published in the Journal of the American Heart Association in October 2025. The researchers reviewed 155 studies and demonstrated consistent, significant associations between viral infections and later cardiovascular events. Acute infections such as influenza and SARS-CoV-2 were linked to sharply elevated short-term risks—up to a four-fold increase in myocardial infarction (heart attack) and a five-fold rise in stroke within the first month after infection. Long-term infections including HIV, hepatitis C, and herpes zoster were likewise associated with higher levels of risk for coronary heart disease (CHD) and stroke.

The authors conclude that viral infections “represent underrecognized and potentially preventable contributors” to global CVD burden. This emerging scientific consensus effectively reframes chronic disease as, in many cases, the delayed consequence—or sequela—of infection.

Health and Human Services Secretary Robert F. Kennedy Jr. speaks alongside Food and Drug Administration administrator Dr. Martin Makary, left, and Dr. Jay Bhattacharya, director of the National Institutes of Health, as they announce that the government would no longer endorse the COVID-19 vaccine for healthy children or pregnant women. [AP Photo/Health and Human Services]

Yet this paradigm shift stands in sharp contrast to the federal public health policy announced by right-wing anti-science quack Robert F. Kennedy Jr., placed in charge of the Department of Health and Human Services by Donald Trump. Kennedy publicly vows to combat chronic disease while simultaneously advancing anti-vaccine positions, dismantling vaccine-advisory structures, and reducing investment in immunization and other methods of prevention of infectious disease. By separating vaccination and infection surveillance from chronic-disease prevention, Kennedy repudiates the very scientific linkage now being illuminated between infection and non-communicable illness—with profound implications for public health.

Acute and chronic viral infections as major cardiovascular risk factors

The UCLA team’s meta-analysis delineates two interrelated dimensions of viral impact on cardiovascular health: acute short-term risk following infection and chronic, long-term burden stemming from persistent viral disease.

Chart shows impact of infections on chronic disease risk [Photo: UCLA study]

For acute infections, the evidence was striking. Laboratory-confirmed influenza infection was linked to a four-fold increase in heart attacks and a five-fold increase in strokes within the first month after infection. Likewise, COVID-19 showed consistent and pronounced cardiovascular effects. During the first 14 weeks after infection, the risk of myocardial infarction or stroke was roughly three times higher compared with uninfected individuals, with elevated risk persisting up to one year. Long-term follow-up indicated a 74 percent higher risk of CHD and a 69 percent higher risk of stroke among those previously infected. As researchers noted, infections like COVID are “the visible tip of an iceberg,” triggering inflammatory and vascular damage across multiple organ systems, with the cardiovascular system bearing a disproportionate burden. These findings reinforce the necessity of preventive interventions—especially vaccination—to mitigate infection-driven cardiovascular disease.

The study also established that viral infections can produce enduring cardiovascular harm. HIV infection was associated with a 60 percent long-term increase in CHD risk, 45 percent higher stroke risk, and nearly double the risk of heart failure. Hepatitis C virus (HCV) conferred a 27 percent higher risk of CHD and 23 percent higher risk of stroke. Reactivation of varicella-zoster virus (herpes zoster) was linked to elevated CHD and stroke risks lasting up to a decade after infection.

This pattern underscores that viral infections amplify cardiovascular vulnerability across populations—but most acutely among those already burdened by preexisting risk factors or limited access to healthcare. As with many infectious and chronic diseases, the intersection of biological and social determinants means that low-income communities and populations in low- and middle-income countries bear the greatest cumulative risk.

Infections as upstream drivers of chronic disease

Beyond cardiovascular pathology, a wide spectrum of cancers, autoimmune conditions, and neurological disorders are now understood to be initiated or accelerated by infectious agents. A 2020 Lancet Global Health modeling study estimated that 130 million disability-adjusted life years (DALYs) from non-communicable diseases—8.4 percent of the total global NCD burden—are attributable to infection, acknowledging this as a conservative lower bound.

A wide range of research, coupled with the 2025 UCLA findings on viral infections and CVD, underscores a single, powerful conclusion: many so-called “non-communicable” diseases are conditions derived from the long-term health effects of communicable diseases.

Florida seniors have their temperatures taken before receiving the second dose of the Pfizer COVID-19 vaccine at Jackson Health System in Miami [Credit: AP Photo/Marta Lavandier]

This reconceptualization has profound policy implications. Recognizing that chronic disease frequently arises from infectious origins opens a path to preventing irreversible outcomes by interrupting infection early. The historical precedent is instructive: when the bacterial cause of peptic ulcer disease was finally accepted in the 1980s, it overturned decades of dogma attributing ulcers to stress or lifestyle and revolutionized treatment through antibiotics. Today, the emerging infection-NCD paradigm demands a similar transformation—one that integrates vaccination, surveillance, and pathogen elimination directly into chronic-disease prevention frameworks.

Vaccination must therefore be repositioned not merely as an acute-disease intervention but as a foundational pillar of cardiovascular and chronic-disease care, alongside blood-pressure control, lipid management, and smoking cessation. Any policy that undermines vaccination or infectious-disease control strikes at the heart of chronic-disease prevention itself.

COVID-19 pandemic as a case study of the “let-it-rip” policy

The COVID-19 pandemic offers a sobering large-scale case study of how a single infectious agent can generate a massive non-communicable-disease burden at the population level. In the United States, confirmed COVID-19 deaths exceeded 1.2 million by October 2024. Yet this figure captures only part of the health crisis. The pandemic’s true toll must be measured through excess mortality—the number of deaths from all causes above what would have been expected based on pre-pandemic trends.

Between 2020 and 2023, the United States experienced roughly 3.63 million excess deaths: approximately 1.01 million in 2020, 1.10 million in 2021, 820,000 in 2022, and 705,000 in 2023. During the first year alone (March 2020–February 2021), a National Bureau of Economic Research analysis estimated 646,514 excess deaths, with 83.4 percent directly attributed to COVID-19. While some excess mortality arose from indirect causes—such as delayed cardiac care, stroke interventions, and rising overdoses—substantial evidence indicates that infection-related cardiovascular and metabolic complications also contributed to these elevated deaths.

Excess deaths in the US during the initial stages of the CoVID pandemic. [Photo: Our World in Data]

Even as acute viral mortality declined, the overall death rate remained abnormally high. By 2023, COVID-19 had fallen to the tenth leading cause of death in the United States, yet total mortality levels remained markedly elevated—far higher than in peer high-income nations. This sustained excess reflects both the long-term sequelae of infection and a weakened public-health infrastructure unable to manage the transition from acute crisis to chronic-disease control.

The so-called “let-it-rip” approach, characterized by premature reopening, minimal infection-control measures, and an emphasis on “personal responsibility” over collective protection, effectively allowed uncontrolled viral spread. This strategy, rooted in the false premise that population immunity through mass infection would end the pandemic, has instead left an enduring legacy of preventable death, disability, and chronic illness. The COVID-19 case demonstrates that infectious-disease policy and chronic-disease prevention cannot exist in isolation: they are two faces of the same public-health imperative.

Cardiovascular mortality reversal during the COVID-19 pandemic

A critical component of the pandemic’s excess mortality is the surge in cardiovascular deaths, marking a reversal of decades of progress in US heart-disease prevention. Between 2020 and 2022, researchers estimated 228,524 excess cardiovascular deaths—about 9 percent more than expected based on pre-pandemic trends. The increase was not evenly distributed: younger adults experienced the sharpest relative rise. By the second year of the pandemic, the observed-to-expected heart-attack mortality rate had jumped 29.9 percent among adults aged 25–44, compared with 13.7 percent among those 65 and older. Such findings strongly indicate that the direct vascular and inflammatory effects of SARS-CoV-2 amplified existing cardiovascular risk, even within populations traditionally considered low-risk for acute coronary events.

Although the federal public-health emergency formally ended in 2023, COVID-19 continues to exact a mortality toll comparable to major injury causes such as automobile crashes. As of 2024, confirmed US COVID-19 deaths still number roughly 50,000–60,000 per year, according to CDC reporting. Yet these figures represent a significant undercount: with only 27 of 50 states maintaining consistent reporting, analysts estimate that the true annual toll is about 36 percent higher—between 78,000 and 94,000 deaths. Even the lower range equals or exceeds a severe influenza season (typically 30,000–50,000 deaths).

This ongoing mortality—occurring alongside the continued rise in cardiovascular deaths—underscores the long-term, infection-mediated burden left in the pandemic’s wake and the failure of “post-emergency” policies to address it as an ongoing public-health crisis.

Long COVID and the infection-driven surge in chronic disease

The continuing elevation in US mortality points to a hidden epidemic of Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC). Far from being limited to lingering fatigue or “mild” symptoms, Long COVID encompasses sustained organ injury and elevated chronic-disease risk across multiple systems. It represents not merely the aftermath of infection but the creation of a new population-level burden of non-communicable disease.

Long COVID has been consistently associated with increased incidence of cardiovascular disease, stroke, diabetes, kidney impairment, and autoimmune disorders. According to modeling from the Pandemic Mitigation Collaborative, the average American has now experienced approximately 4.7 SARS-CoV-2 infections, implying more than 1.6 billion cumulative infections and reinfections in the US alone. This staggering exposure base ensures that even relatively small per-infection risks translate into a vast chronic health impact.

The defining body of evidence emerged from the Veterans Affairs national healthcare database, analyzed in a series of landmark studies by Dr. Ziyad Al-Aly and colleagues. Tracking millions of patients for years, these studies showed that even a single infection sharply increases the risk of death and long-term sequelae across organ systems. In pooled analyses, individuals four weeks or more after acute infection faced a six-fold higher risk of myocarditis, a three-fold increase in thromboembolic events, and roughly double the risk of heart failure and stroke compared with uninfected individuals.

Dr. Ziyad Al-Aly [Photo by Dr. Ziyad Al-Aly]

Subsequent research across independent cohorts has confirmed and extended these findings. A 2024 UK Biobank study reported that post-COVID cardiovascular risk was comparable in magnitude to having type 2 diabetes or peripheral artery disease, highlighting that infection itself functions as a chronic-disease trigger. Likewise, multiple cohort studies demonstrated that COVID-19 survivors have significantly greater odds of developing new-onset metabolic disease—notably type 2 diabetes—and autoimmune conditions such as rheumatoid arthritis and systemic lupus erythematosus within six months after infection.

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