When Will COVID-19 End?

Not since the Spanish flu pandemic of 1918 has there been a global health emergency like COVID-19. The earlier event, which lasted from March 1918 to December 1920, ended up infecting 500 million people and killing roughly 17.4 million worldwide. Efforts to avoid a similar calamity have led to unprecedented calls for social distancing, mandatory lockdowns, and the closure of schools and businesses to attempt to limit COVID-19 infections.

With states now starting to "flatten the curve" on their infection rates, many are looking ahead to bigger questions, including when and how the shutdowns will end, whether the disease will re-emerge, and when scientists will be able to officially declare that COVID-19 is no longer a public health emergency.

when will covid-19 end
Verywell / Hugo Lin

Ending the Lockdowns

Given that little was known about COVID-19 when the disease was first identified, public health authorities had no other choice but to declare a state of emergency when the epidemic blossomed into a full-blown pandemic on March 11, 2020. This included issuing mandatory stay-at-home orders and travel restrictions.

With evidence that the lockdowns have begun to stem the spread of infection—avoiding earlier predictions of 2.2 million American deaths if nothing was done —health officials now have to grapple with how to lift the orders in a way that allows businesses to open and people to return to normal life without risking a rebound in infections.

State Guidance

As with the initial stay-at-home orders, the protocols to lift state and municipal lockdowns have varied by location. While some governors have already taken steps to open parks and certain businesses, others are erring on the side of caution and taking a longer-term view.

Among those calling for a measured approach is California Governor Gavin Newsom who, on April 14, issued six criteria that must be met before mandated restrictions can be lifted in their entirety:

  1. Systems must be in place to test and trace the sources of infection and to support those who have been infected or exposed.
  2. Systems must be in place to prevent infection in older people and those at risk of severe illness.
  3. State and municipal leaders must ensure that hospitals and health systems are able to handle a sudden surge in new infections.
  4. The ability to develop effective therapeutics to ease symptoms and help recovery. They must be able to meet public demand.
  5. Businesses, schools, and child care facilities must adhere to social distancing guidelines.
  6. The state must have the ability to identify when to re-impose restrictions and stay-at-home orders if and when needed.

Until these criteria are met, some level of restriction on public dining, socializing, conference and sports gatherings, and classroom sizes will be maintained in California. The directive more or less aligns with those issued by the World Health Organization (WHO) on the same day.

White House Guidance

The White House issued its "Guidelines for Opening Up America Again" on April 16. The White House plan was more specific in its timeframe, allowing legislators to reopen schools and businesses before May 1 based on a sustained decline in new infections over a 14-day period (referred to as the "gating criteria"). The plan places the burden of testing, contact tracing, and keeping hospitals equipped on states.

With each 14-day decline in the infection rate, the White House advised state and civic leaders to lift their shutdowns in three phases:

  • Phase 1: If the initial gating criterium is met, gatherings of up to 10 are allowed. Restaurants, movie theaters, sporting venues, and places of worship can reopen if sanitation and social distancing measures are in place. "Telework" and a limitation on business travel would be encouraged. Schools, daycare, camps, and common work areas would remain closed, and visits to elder care facilities would still be banned.
  • Phase 2: If gating criterium is met for a second two-week period, gatherings of up to 50 are allowed. Schools, camps, and child care facilities can reopen. The elderly and medically vulnerable populations would still be encouraged to shelter at home. Non-essential travel could resume.
  • Phase 3: If gating criterium is met for another two weeks, workplace restriction can be lifted. Visits to elder care facilities could resume with the appropriate hygiene measures in place. The elderly and other medically vulnerable people can resume public interactions with appropriate hygiene and social distancing practices.

States themselves ultimately have the say on whether they follow these guidelines and when to open.

Both the White House and California approaches have their supporters and detractors and raise reasonable questions as to their implications and risks.

With the California plan, it is unclear what would constitute developing an "effective treatment" and with the White House plans, it is unclear if Phase 3 would allow for packed stadiums or what risks unimpeded travel might have on disease re-emergence.

Risk of Future Outbreaks

As researchers struggle to make sense of COVID-19, many have begun to look back on lessons learned from earlier pandemics.

While COVID-19 and the Spanish flu are different entities and don't even belong to the same family of viruses, they share similarities in their modes of transmissions and the ways in which the immune system responds to them.

Lessons from the Spanish Flu

During the Spanish flu pandemic of 1918, the disease hit the global community in waves. The first wave in the spring of 1918 was not unlike what you would expect of annual influenza, with similar rates of infection and death. By August of that year, a second, deadlier wave struck, following World War I troop movements across Europe, Russia, Asia, Africa, Australia, and the Americas. After the premature lifting of national quarantines in January 1919, a third wave hit. Health officials declared control in December 1920.

The Spanish flu is believed to have been caused by sudden mutations of the H1N1 virus, which some say occurred between the first and second waves, likely in the United States. The eventual disappearance of Spanish flu may be the result of mutations that weakened the virus but are more likely due to adaptive herd immunization in which exposure to the virus provided immunity to large sectors of the population.

Adaptive immunity is a type of immunity that develops in response to an infection. After an infection has been cleared, the body will leave behind immune cells (called memory B-cells) that watch for the return of the disease and act quickly when it does. Herd immunity applies this adaptive immunity to a group of people.

Adaptive herd immunity is evidenced in part by historic records in which Copenhagen, a city hard-hit by the first wave of H1N1, emerged from the Spanish flu pandemic with a fatality rate of 0.29%, roughly 10 times less than the death rate experienced elsewhere.

Expectations With COVID-19

While it is too early to suggest that the same patterns might emerge with COVID-19, experience with the Spanish flu and other strains of coronavirus outbreaks (including SARS in 2003 and MERS in 2012, 2015, and 2018) suggests that adaptive immunity will play a central role in whether the disease will rebound, and to what level.

With Spanish flu, adaptive herd immunization afforded those who survived infection an immune defense against the virus if re-exposed. There is evidence that the same would occur in those infected during the current COVID-19 pandemic.

According to research from the Chinese Academy of Medical Science, monkeys infected with COVID-19 were not able to be re-infected when exposed to a second dose of the virus.

This shouldn't imply that COVID-19 will act in the exact same way or that widespread herd immunization—a tactic initially pursued by the United Kingdom and actively pursued in Sweden—is a reasonable option given what little we know about COVID-19.

There is, in fact, evidence that coronaviruses are able to target and kill many of the front-line cells that give rise to adaptive immunity, suggesting that reinfection is possible, at least in some people.

What it does suggest is that the burden of control is placed on widespread shelter-in-place policies, which aim to stop infections from occurring, or a vaccine should the virus re-emerge.

What the Second Wave May Look Like

Looking ahead, public health officials are preparing for the return of COVID-19 in the latter part of 2020. How this second wave might present itself is open to speculation. It is not entirely unreasonable to suggest that future outbreaks may be less severe, in part because herd immunity, whether intentional or not, will likely have afforded large sectors of the population with immunization.

Moreover, COVID-19 does not appear to mutate as quickly as influenza, meaning that it is less of a "moving target" for vaccine developers and may not require a new vaccine each and every year. At the same time, it means that is unlikely that COVID-19 will mutate into a less severe strain anytime soon.

Something that could complicate a second wave is if it were to coincide with the outbreak of seasonal flu. There is early evidence of co-infection of COVID-19 and influenza in a 69-year-old man in China this January. While co-infection is still considered uncommon, the Chinese investigation revealed that it may simply be under diagnosed due to difficulties in differentiating the co-occurring viruses.

Furthermore, it is unknown if co-infection would inherently make respiratory symptoms worse, although this could be likely if the upcoming influenza strain is particularly virulent and capable of attaching to cells in the lower respiratory tract (rather than the upper respiratory tract, as it more often does). H1N1 influenza, associated with both Spanish flu and the swine flu pandemic of 2009, is one such subtype known to behave in this way.

Health Advisory

Given the likelihood of a return of COVID-19 during flu season 2020-2021, it is doubly important to get your annual flu shot, typically around October unless your doctor tells you otherwise.

Ending the Pandemic

Given what we know about COVID-19, there are two main ways that the pandemic can either be stopped or controlled. The first scenario is to implement even stricter public health measures to stop all infections from occurring. The second is to develop a vaccine.

Policy Challenges

Strict public health measures ultimately ended the SARS epidemic of 2003 (which ended up killing 774 people with a fatality rate of 9%). By acting quickly and limiting the spread of infection, health officials were able to force the virus into retreat. With no hosts to infect, the virus quickly died out and has not been seen since 2004.

However, given the global spread of the COVID-19 (and evidence that the virus may be more transmissible than SARS), it is unlikely that the same approach would work today. That leaves the development of a vaccine as the top priority among researchers and health officials.

Vaccine Challenges

In an ideal world, a COVID-19 vaccine would deliver levels of immune protection at least equal to that of the annual quadrivalent flu vaccine (roughly 45%). Note: This rate varies year-by-year and is sometimes much higher than 45%. Even if efficacy levels are considerably low, the vaccine might still be considered viable for the elderly and other high-risk groups.

A major challenge to the development of a vaccine is the structure of the virus itself. COVID-19 is classified as a positive-sense single-stranded RNA virus alongside the SARS virus, MERS virus, hepatitis C virus (HCV), West Nile virus (WNV), and dengue virus. Of these, only dengue fever has an effective vaccine.

By contrast, the development of a MERS vaccine (likely the model many scientists will base their designs on) has been hindered by the lack of an immune response where it is needed most, namely in the mucosal tissues of the upper respiratory tract. A generalized immune response, while useful, may not be enough to prevent COVID-19 from attaching to local respiratory cells and causing infection. This lesson was learned from recent vaccine failures, including ones that were intended to prevent respiratory syncytial virus (RSV).

This is not to suggest that the development of a COVID-19 vaccine will be slow or drag on for years or decades. There have, in fact, been advances with the MERS vaccine in recent years, and aggressive funding may incentivize greater global collaboration.

But, even with the fast-tracking of human clinical trials, any suggestion that a vaccine will be market-ready in 18 months is likely overly-optimistic. Ultimately, whichever candidate emerges as frontrunner will have to overcome multiple hurdles before it can be approved.

For a COVID-19 vaccine to be considered viable, it would need to be safe, easy to deliver (ideally with a single dose), affordable, transportable, stable, and able to be produced quickly on a global scale.

Filling Gaps in Research

In the absence of a COVID-19 vaccine, even a modestly effective one, the only thing that may alter the course of public policy is research. This would require, among other things, a true fatality rate and an accurate disease prevalence (the number of cases in a particular population at a given time).

Estimating these things at the height of a pandemic is difficult and can cause misconceptions and cast doubt in the public as reports are continuously updated and data constantly changed. While initial data from Wuhan, China, for example, cited the COVID-19 fatality rate at 5.45%, subsequent studies have pegged the rate closer to 1.4%. There have been suggestions that the rate may even be lower.

These statistical changes are neither contradictory nor the result of flawed research. It is simply that testing efforts, particularly in the U.S., have been mainly constrained to those who are sick or hospitalized. As of yet, it is unknown how many asymptomatic (symptom-free) or subclinical (minimally symptomatic or asymptomatic) infections there are in comparison to confirmed ones.

Some researchers suggest that for every confirmed COVID-19 case, there are 5 to 10 that are either asymptomatic/minimally symptomatic and undiagnosed. If so, the roughly 750,000 infections reported in the U.S. in the latter half of April may be closer to 4 million, 8 million, or more.

Other studies contend that the actual infection rate may be as much as 100 times higher in certain hotspots, a theory which may prove eerily correct given early reports that 1 in 7 New York City residents may already be infected.

If correct, the actual number of cases in New York City may be closer to 1.8 million in contrast to the 145,000 currently reported.

While changes like these would significantly decrease the fatality rate among Americans, it would likely do little to sway public policy for the short to medium term. Even if the 5% fatality rate frequently reported in the media were to drop to, say, 1% (a figure more closely aligned to the NIH estimates), that would still be 10 times higher than the 0.1% fatality rate seen with the flu.

With broader testing and a clearer picture of the prevalence of COVID-19, health officials can begin to assess how realistic alternative interventions (such partial or regional shutdowns) may be.

A Word From Verywell

As challenging as the COVID-19 pandemic has been for many, patience and vigilance are the two things that will see you through the coming months and years. Rather than worrying about whether the pandemic will return, do your best to adhere to public health guidelines and protect yourself from infection by keeping healthy, maintaining good hygiene practices, and getting your annual flu shot.

With time and persistence, the world community will eventually turn the corner on this global pandemic.

The information in this article is current as of the date listed, which means newer information may be available when you read this. For the most recent updates on COVID-19, visit our coronavirus news page.

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28 Sources
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  1. Spreeuwenberg P, Kroneman M, Paget J. Reassessing the global mortality burden of the 1918 influenza pandemic. Am J Epidemiol. 2018;187(12):2561-7. doi:10.1093/aje/kwy191

  2. Cucinotta D, Vanelli M. WHO Declares COVID-19 a Pandemic. Acta Biomed. 2020;91(1):157-60. doi:10.23750/abm.v91i1.9397

  3. Imperial College COVID-19 Response Team. Report 9: Impact of non-pharmaceutical interventions (NPIs) to reduce COVID-19 mortality and healthcare demand.

  4. Woolfolk J. Coronavirus: What must happen before California reopens. Mercury News.

  5. World Health Organization. COVID‑19 strategy update - 14 April 2020.

  6. White House. Guidelines for Opening Up America Again.

  7. Martini M, Gazzaniga V, Bragazzi NL, Barberis I. The Spanish influenza pandemic: A lesson from history 100 years after 1918. J Prev Med Hyg. 2019;60(1):E64-7. doi:10.15167/2421-4248/jpmh2019.60.1.1205

  8. Taubenberger JK, Baltimore D, Doherty PC, et al. Reconstruction of the 1918 influenza virus: unexpected rewards from the past. mBio. 2012;3(5):00201-12. doi:10.1128/mBio.00201-12

  9. Andreasen V, Viboud C, Simonsen L. Epidemiologic characterization of the 1918 influenza pandemic summer wave in Copenhagen: implications for pandemic control strategies. J Infect Dis. 2008;197(2):270-8. doi:10.1086/524065

  10. Wang Y, Sun J, Zhu A, Zhao J, Zhao J. Current understanding of Middle East respiratory syndrome coronavirus infection in human and animal models. J Thorac Dis. 2018;10(Suppl 19):S2260-71. doi:10.21037/jtd.2018.03.80

  11. Bao L, Deng W, Gao H. Reinfection could not occur in SARS-CoV-2 infected rhesus macaques. BioRXiv. 2020 Mar 14[Online ahead of print]. doi:10.1101/2020.03.13.990226

  12. Mesel-Lemoine M, Millet J, Vidalain PO, et al. A human coronavirus responsible for the common cold massively kills dendritic cells but not monocytes. J Virol. 2012;86(14):7577-87. doi:10.1128/JVI.00269-12

  13. Kupferschmidt K. Genome analyses help track coronavirus' movesScience. 2020 Mar;367(6483):1176-77. doi:10.1126/science.367.6483.1176

  14. Wu X, Cai Y, Huang X, et al. Co-infection with SARS-CoV-2 and influenza A virus in patient with pneumonia, China. Emerg Infect Dis. 2020;26(6)[Online ahead of print]. doi:10.3201/eid2606.200299

  15. Camp JV, Bagci U, Chu YK, et al. Lower respiratory tract infection of the ferret by 2009 H1N1 pandemic influenza A virus triggers biphasic, systemic, and local recruitment of neutrophils. J Virol. 2015;89(17):8733-48. doi:10.1128/JVI.00817-15

  16. Prompetchara E, Ketloy C, Palaga T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac J Allergy Immunol. 2020;38(1):1-9. doi:10.12932/AP-200220-0772

  17. Andersen KG, Rambaut A, Lipkin WI, Holmes EC, Garry RF. The proximal origin of SARS-CoV-2Nature Med. 2020;26:450-2. doi:10.1038/s41591-020-0820-9

  18. Dawood FS, Chung JR, Kim SS, et al. Interim estimates of 2019–20 seasonal influenza vaccine effectiveness — United States, February 2020. MMWR. 69(7);177-82.

  19. Yong CY, Ong HK, Yeap SK, Ho KL, Tan WS. Recent advances in the vaccine development against Middle East respiratory syndrome-coronavirus. Front Microbiol. 2019;10:1781. doi:10.3389/fmicb.2019.01781

  20. Mazur NI, Higgins D, Nunes MC, et al. The respiratory syncytial virus vaccine landscape: lessons from the graveyard and promising candidates. Lancet Infect Dis. 2018 Oct 1;18(10):E295-311. doi:10.1016/S1473-3099(18)30292-5

  21. Yang S, Cao P, Du P, et al. Early estimation of the case fatality rate of COVID-19 in mainland China: a data-driven analysis. Ann Transl Med. 2020;8(4):128. doi:10.21037/atm.2020.02.66

  22. Wu JT, Leung K, Bushman M, et al. Estimating clinical severity of COVID-19 from the transmission dynamics in Wuhan, ChinaNat Med. 2020;26:506-10. doi:10.1038/s41591-020-0822-7

  23. Li R, Pei S, Chen B, et al. Substantial undocumented infection facilitates the rapid dissemination of novel coronavirus (SARS-CoV2). Science. 2020 Mar 16[Online ahead of print]. doi:10.1126/science.abb3221

  24. Centers for Disease Control and Prevention. Cases of coronavirus disease (COVID-19) in the US.

  25. Silverman JD, Hupert N, Washburne AD. Using ILI surveillance to estimate state-specific case detection rates and forecast SARS-CoV-2 spread in the United States. MedRXiv. 2020 Apr 14[Online ahead of print]. doi:10.1101/2020.04.01.20050542

  26. CNBC. New York antibody study estimates 13.9% of residents have had the coronavirus, Gov. Cuomo says.

  27. Mooney C, Eliperin J, Achenbach J. As U.S. coronavirus fatality rate rises to 5 percent, experts are still trying to understand how deadly this virus is. Washington Post.

  28. Rajgor DD, Lee MH, Archuleta S, Bagdasarian N, Quek SC. The many estimates of the COVID-19 case fatality rate. Lancet Infect Dis. 2020 Mar 27[Online ahead of print]. doi:10.1016/S1473-3099(20)30244-9