Is COVID-19 Back? What’s Happening Right Now

COVID-19 never truly disappeared. The virus settled into a pattern familiar to other respiratory infections: seasonal waves, ongoing variant evolution, and periodic surges that catch public attention before fading from the news cycle. What has changed is the backdrop. Population-level immunity from vaccination and prior infection has blunted the worst outcomes for most people, but new subvariants keep finding ways around that immunity, and the groups left most vulnerable have shifted. Meanwhile, the global surveillance infrastructure that tracked the virus so closely during the pandemic has contracted sharply, making it harder to know exactly what is circulating at any given moment.

The Variant Landscape Has Not Settled Down

SARS-CoV-2 continues to mutate at a pace that surprises even seasoned virologists. The Omicron lineage (B.1.1.529), which emerged in late 2021, has branched into dozens of subvariants, and these keep displacing one another. Descendants of the BA.2.86/JN.1 branch, including KP.2, KP.3, and their sub-lineages, became globally dominant in 2024 and showed substantially reduced sensitivity to antibodies generated by earlier vaccines and infections. Sera from vaccinated individuals and convalescents showed a clear drop in neutralizing activity against JN.1, KP.2, and related variants compared to older Omicron lines.¹ Lab studies of JN.1-derived subvariants like LB.1, KP.2.3, KP.3, and KP.3.1.1 confirmed that all are highly evasive of antibodies raised by bivalent mRNA vaccines, XBB.1.5 monovalent vaccines, and BA.2.86/JN.1-wave infections. Much of that escape traces to a single deletion in the spike protein’s outer domain.²

The most recent variant to attract global attention is BA.3.2, nicknamed “Cicada,” which received World Health Organization Variant Under Monitoring status in December 2025. BA.3.2 did not descend neatly from the JN.1 branch. Instead, it emerged without a clear intermediate lineage, a pattern suggesting it evolved during a prolonged, unmonitored infection in a single host before spilling back into the wider population.³ Lab work found that BA.3.2 evades neutralizing antibodies from bivalent mRNA vaccination, Omicron BA.1-wave infection, and JN.1-wave infection with a dramatic reduction in antibody effectiveness. It achieves this partly by adding new sugar-coated shields on the spike protein’s surface, but that trick comes at a cost: when those sugar sites are disrupted, the virus becomes more infectious and more vulnerable to antibodies again. This tradeoff between immune evasion and raw infectivity is characteristic of the evolutionary pressure SARS-CoV-2 faces.⁴

Why Your Immunity Keeps Fading

Two forces work against lasting protection. The first is that antibodies simply decline over time. Neutralizing antibodies induced by mRNA vaccines drop noticeably within three to six months after a dose.⁵ A large meta-analysis quantified this: in people who had been vaccinated but never infected, antibodies against the original strain fell roughly five-fold in the six months after a primary course, and about four-fold after a booster over the same period.⁶ A booster restores levels temporarily, but the trajectory is the same: a peak followed by a steady decline.

The second force is antigenic drift. Even if your antibody levels were high, the virus has changed enough that those antibodies recognize it less well. Each new round of spike mutations erodes the match between your immune memory and the circulating variant. This is not unique to COVID-19; influenza does the same thing, which is why flu shots are updated annually. The practical effect is that a person who was vaccinated or infected a year ago may still have strong T-cell responses that prevent severe illness but weaker antibody responses that do not block infection altogether.

Seasonal Waves Are Now the Norm

COVID-19 mortality follows a winter pattern much like other respiratory illnesses, with peaks in cold months and troughs in summer.⁷ In practice, the United States and much of the Northern Hemisphere see a late-fall or winter surge and, in some years, a smaller summer bump. Indoor crowding, lower humidity, and behavioral changes (more time inside with windows closed) all contribute. Improved ventilation has been shown to reduce COVID-19 risk in indoor settings, yet most buildings have returned to pre-pandemic airflow standards.⁸

Wastewater surveillance remains one of the best tools for spotting early surges, since it captures infections in a community regardless of whether people bother to get tested. Tracking viral RNA in sewage reliably reflects the rise and fall of cases in a metropolitan area.⁹ This matters more now because individual testing has plummeted. Far fewer people take rapid tests or report results to public health agencies than they did during 2021 or 2022, so official case counts understate reality. Wastewater data fills some of that gap, but it does not tell you which variant is circulating without additional genomic sequencing.

The Surveillance Problem Nobody Is Talking About

Genomic sequencing, which identifies new variants before they spread widely, has declined steeply. High-income countries submitted twenty-five times fewer sequences per capita in 2024 than in 2022.¹⁰ That is not because the virus stopped evolving. It is because pandemic-era funding dried up, political will evaporated, and public health agencies redirected resources. The consequence is a longer blind spot. On average, once a new Omicron subvariant emerges, it takes about a month to reach a new region, then another week or two to be diagnosed, and another week or two after that to be sequenced and identified.¹¹ With fewer labs doing sequencing, those lags stretch further. BA.3.2 emerged without a known intermediate lineage, suggesting it circulated undetected for an extended period, a scenario that becomes more likely as sequencing shrinks.³

Who Is Still Getting Seriously Ill

For most healthy adults who have been vaccinated or previously infected, a COVID-19 infection in the Omicron era is unpleasant but manageable. The people filling hospital beds look different from the early pandemic days. Among adults hospitalized with COVID-19 in a twelve-state U.S. surveillance network during the 2023–2024 season, about 80% had at least two underlying medical conditions, roughly 18% needed intensive care, about 8% required a ventilator, and about 7% died during hospitalization.¹² The profile is clear: COVID-19 hospitalizations now concentrate heavily among older adults and people with chronic conditions.

Immunocompromised individuals face the sharpest risk. A meta-analysis covering the Omicron era found that organ transplant recipients had nearly seven times the risk of death and hospitalization compared to people without immune-suppressing conditions.¹³ Solid organ transplant recipients carry especially elevated risk, and that risk is highest in the period soon after transplant surgery and among kidney and lung recipients.¹⁴ For these patients, remdesivir given within the first two days of hospitalization was associated with roughly a 25% reduction in mortality at both 14 and 28 days, and the benefit held across subgroups with cancer and blood cancers.¹⁵

Children and COVID-19 Now

Pediatric COVID-19 is generally mild, but hospitalizations still happen, and the children admitted to hospitals tend to share certain features. Among roughly 2,500 children hospitalized for COVID-19 in a U.S. network between 2022 and 2024, nearly 45% were between 6 and 23 months old, and about 59% overall had at least one underlying condition. Chronic lung disease, cardiovascular disease, diabetes, and neurologic disorders were all linked to more severe outcomes. Strikingly, only about 4% of these hospitalized children were up to date on recommended COVID-19 vaccination.¹⁶ Fever was the most common symptom in hospitalized children (about 79%), followed by poor feeding, gastrointestinal symptoms, and cough.¹⁷

Updated Vaccines and What They Actually Do

Vaccine manufacturers have been chasing the virus with updated formulations. Variant-adapted boosters targeting BA.1 or XBB.1.5 produced higher antibody levels against their matched variants than the original formulation did. In one trial, previously vaccinated adults who received a BA.1-adapted shot had roughly three times the neutralizing antibody response against Omicron BA.1 compared to those who received the original booster.¹⁸ A comparison of different booster platforms found that bivalent mRNA vaccines produced the highest levels of cross-reactive antibodies against newer subvariants like EG.5, JN.1, and KP.2, even though those variants had not yet emerged when the boosters were given.¹⁹

Real-world data from England showed that a booster dose provided roughly 97% to 99% protection against hospitalization or death for at least ten weeks, regardless of which primary vaccine series someone had received.²⁰ That protection erodes over time, as discussed above, but the takeaway is that a recent booster still provides strong short-term defense against the worst outcomes. The challenge is getting people to take it. Booster uptake has fallen dramatically since the early rollout. For most adults, the practical question is whether to get the latest available formulation before winter respiratory season. For immunocompromised people and older adults, the answer is almost always yes.

Antivirals Still Work, but Resistance Is on the Horizon

Paxlovid (nirmatrelvir/ritonavir) remains the most widely prescribed outpatient antiviral for COVID-19, and the active ingredient retains potent activity against current variants despite extensive changes in the viral genome.²¹ Real-world data during Omicron waves confirmed that Paxlovid recipients had substantially lower 28-day mortality compared to matched controls, and the drug also appeared to prevent the viral rebound sometimes seen in untreated patients.²²

The worry, though, is resistance. Researchers have identified mutations in the viral protease that nirmatrelvir targets. Some of these mutations also confer cross-resistance to other drugs in the same class, including ensitrelvir and ibuzatrelvir. One triple mutation was highly resistant to all three drugs in lab tests.²³ Separately, analysis of clinical samples found novel resistance mutations that sit far from the drug’s binding site but still disrupt the protein’s shape enough to reduce the drug’s effectiveness, suggesting the virus has multiple evolutionary routes to resistance.²⁴ These resistant forms remain rare in the wild for now, but widespread antiviral use combined with declining surveillance creates conditions where resistant strains could spread without being noticed quickly.

Long COVID in the Omicron Era

One of the persistent worries about repeated COVID-19 infections is long COVID, the constellation of symptoms that can linger for months after the acute illness resolves. The good news is that infections during the Omicron period have been linked to a lower probability of long COVID than infections during earlier waves. One study found that roughly 48% of Omicron-era patients reported lingering symptoms, compared to about 67% during pre-Omicron periods.²⁵ Some of that improvement likely reflects higher population immunity, some may reflect intrinsic differences in the variant, and some reflects reduced disease severity overall.

That said, certain post-infection complications persist. A large study in a highly boosted population found that most organ-system complications were no more frequent in test-positive individuals than in test-negative controls during the Omicron era. The exceptions were kidney complications during the early Omicron BA.1/2 period and, across all variant eras, individual neuropsychiatric outcomes like memory problems and Alzheimer’s disease diagnoses. Loss of smell or taste, once a hallmark of COVID-19, showed increased risk only during the Delta era, suggesting later Omicron variants cause this less often.²⁶

When COVID-19 Meets the Flu or RSV

Respiratory virus season does not neatly sort itself into one pathogen at a time. Co-infections with influenza and SARS-CoV-2 are uncommon but consequential. A meta-analysis found that people co-infected with flu and COVID-19 had roughly double the odds of needing intensive care and mechanical ventilation compared to those with COVID-19 alone.²⁷ A multicenter study covering 2021–2025 confirmed this pattern in adults: co-infected patients had higher odds of hospital admission and more frequent severe outcomes than those with any single virus.²⁸

In children, the picture is slightly different. Among hospitalized kids with SARS-CoV-2, the most common co-pathogens were RSV and rhinovirus/enterovirus, not influenza. RSV co-infection led to more bronchiolitis and hypoxia and a greater need for respiratory support, though rates of invasive ventilation and formally severe COVID-19 were not higher than in children with COVID-19 alone.²⁹ The practical point is that getting vaccinated against both flu and COVID-19 before winter is not redundant. Each vaccine addresses a different virus, and being hit by two respiratory pathogens simultaneously is genuinely more dangerous than dealing with either alone.

Rapid Tests Still Detect Current Variants

A common question when a new variant emerges is whether home rapid antigen tests still work. These tests target the nucleocapsid protein, a part of the virus that has mutated far less than the spike. Lab evaluations have shown that rapid antigen tests reliably detect Omicron, Delta, Alpha, and Gamma variants, though the sensitivity threshold varies by variant.³⁰ The critical variable is timing: tests are most sensitive when taken within the first few days of symptoms, when viral load is highest. A negative test on day one of symptoms does not rule out infection. If you feel sick and the first test is negative, retesting a day or two later meaningfully improves accuracy.

The bigger issue with testing is not whether the technology works but whether people use it. With free test distribution programs winding down in many countries, fewer people have tests on hand when they get sick. This contributes to the overall undercount of cases and makes the virus harder to track at a population level. If you are immunocompromised, over 65, or living with someone who is, keeping a supply of rapid tests at home is a straightforward way to catch an infection early enough for antivirals to help, since Paxlovid works best when started within five days of symptom onset.