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Despite uncertainties around whether some cases are in fact SARS-CoV-2 infections, “long-haulers” such as those in the online group point to the possibility that COVID-19 is not just a transient respiratory disease, but could manifest as neurological and physical symptoms that persist even months after people fall ill. Although many of them may yet recover in the coming months, some scientists are becoming increasingly worried that some may end up with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a debilitating and poorly understood condition associated with some viral infections. In a press conference last week, for instance, National Institute of Allergy and Infectious Diseases Director Anthony Fauci noted that some of the long-haulers’ symptoms resemble those of ME/CFS. Studies are now underway to track whether some long-haulers develop the disease, and if so, to investigate its underlying mechanisms and possible avenues for treatment quickly. 

“This is a massive infection of millions and millions of people. I think one has to be really concerned about the long-term consequences,” notes Avindra Nath, a neurovirologist at the National Institute of Neurological Disorders and Stroke. “A lot of emphasis early on has been on providing treatments and vaccines and antibodies and all that kind of stuff, but the long-term consequences have not received the attention that they deserve.” 

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“Fast forward a month, and the world did have a pandemic on its hands. Modelers around the world scrambled to forecast the spread of SARS-CoV-2 and the COVID-19 disease it causes in their own countries and communities. Many epidemiologists were then and still are tasked by policymakers with answering urgent questions: How fast will it spread? How many hospital beds and ventilators will we need? When can we lift lockdowns and restart our economies again? Will we see a second wave? Will it be worse than the first?

Getting good estimates for R0—a key epidemiological metric that reflects the transmissibility of a virus—is key to answering such questions with accuracy. But R0 is notoriously tricky to nail down. It depends not only on the biological characteristics of a virus—which are a mystery at the beginning of an outbreak—but also on understanding how often people come into contact with one another. Faced with uncertainty, modelers have to make assumptions about the factors that determine human movement, which can limit the precision of their models and the accuracy of the predictions they generate. 

“R0 is a metric that is, first of all, poorly measured. And secondly, it’s informing models that result in public health action,” says Juan B. Gutiérrez, a mathematician at the University of Texas at San Antonio. “If we get it wrong, the public health action will be misplaced.” 

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Image: CannaSafe

Because cannabis is still considered illegal at the federal level, the responsibility of regulating cannabis and cannabis-derived products falls to states, creating a patchwork of different testing requirements across the country. In addition, state governments issue little to no guidance about protocols for testing products for either potency or safety. Instead, labs have had to trailblaze the development of their own methods. 

Now, in a cannabis testing industry that is only a few years old, it’s evident that reports on potency can vary from lab to lab, and recalls of contaminated products happen across the country, threatening consumer trust. “It’s not really at all like any other industry I’ve worked in, in that they’re still trying to work out proficiency and certification standards,” notes Frank Conrad, an analytical chemist formerly in the biofuels industry who now runs Colorado Green Lab, a consultancy firm for the cannabis industry. 

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Image: Birgit Ritschka 

For decades, scientists had ignored senescent cells—which are trapped in a long-term state of cell cycle arrest—dismissing them as artifacts of cell culture with no significance inside living organisms. But in recent years, Kirkland and other researchers have established senescence as an important physiological process that appears to play seemingly opposing roles in vivo. On the one hand, senescent cells are thought to mediate tissue development when they form in the embryo, and also to promote tissue regeneration and wound repair in later life. However, as these zombie cells accumulate with age, they can ooze inflammatory proteins believed to cause tissue dysfunction and to push neighboring cells into senescence. Indeed, animal studies have suggested that destroying senescent cells can slow down age-related physical decline and boost overall health, and many researchers who study aging now regard senescence as a driver of the physical decline characteristic of old age and a contributor to a range of age-related diseases.

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Image: CDC/Dr. Fred Murphy

Like many other respiratory conditions, COVID-19—the disease caused by SARS-CoV-2—can vary widely among patients. The vast majority of confirmed cases are considered mild, involving mostly cold-like symptoms to mild pneumonia, according to the latest and largest set of data on the new coronavirus outbreak released February 17 by the Chinese Center for Disease Control and Prevention.   

Fourteen percent of confirmed cases have been “severe,” involving serious pneumonia and shortness of breath. Another 5 percent of patients confirmed to have the disease developed respiratory failure, septic shock, and/or multi-organ failure—what the agency calls “critical cases” potentially resulting in death. Roughly 2.3 percent of confirmed cases did result in death.  

Scientists are working to understand why some people suffer more from the virus than others. It is also unclear why the new coronavirus—like its cousins SARS and MERS—appears to be more deadly than other coronaviruses that regularly circulate among people each winter and typically cause cold symptoms. “I think it’s going to take a really, really long time to understand the mechanistic, biological basis of why some people get sicker than others,” says Angela Rasmussen, a virologist at Columbia University’s Mailman School of Public Health.  

In the meantime, the latest data from China and research on other coronaviruses provide some hints. 

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Image: Pirbright Institute

In 2018, China reported an outbreak of the Georgia 2007 strain in Shenyang, a city in the country’s northeast. From there, it swept through the world’s largest congregations of pigs and among countless small farms, killing hundreds of thousands of animals across China. By the end of October 2019, nearly 200 million animals had been culled in a desperate effort to stop the virus, but ASFV continued to spread, popping up in Mongolia, Vietnam, Cambodia, Laos, Myanmar, South Korea, and the Philippines. In October, Mark Shipp, the president of the World Council of Delegates of the World Organization for Animal Health, told reporters that around a quarter of the global pig population could die due to the disease. 

Unrelated to the East Asian epidemic, new outbreaks have also been reported in Eastern Europe. There, low levels of the virus have been circulating in wild boar and domestic pig populations for more than a decade since it arrived from its native Africa, where it often leaps from wild pigs to domestic animals. The rapid spread of ASFV across Eastern Europe and Asia alarmed officials in Asia, Western Europe, and North America, concerned that the virus could slip into their countries via contaminated pork products or animal feed imported from infected countries. Seemingly overnight, finding a vaccine for ASFV—a virus that had long stood at the periphery of the scientific community’s attention—became a global research priority.

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Image: Mathias Appel / Wikimedia Commons

The realization that such contagious cancers may be more widespread than previously thought has intensified efforts to understand their biology—not just for the sake of the species they affect, but also to understand how cancer can become an infectious disease. Many questions remain unanswered, including how these diseases emerge and in what populations. But in the last few years, genetic and immunological studies have provided some insight into these cancers’ interactions with their hosts. The findings have led researchers to view them as independent parasites, with the survival of their host species depending on a delicate interplay between the animals’ immune systems and the cancers’ ability to evade them.

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Image: Faraj Meir/Wikimedia

Chinese white dolphins, like other cetacean species, use songs and whistles to communicate while resting, socializing, and feeding. But after analyzing the whistles from the central group, Pine and his colleagues found that they were significantly longer and much more complex than calls the researchers were more familiar with. The recorded sounds included a greater number of inflection points, where the pitch of the whistles changed abruptly. This heightened complexity signifies that the dolphins were communicating a greater amount of emotional information, the researchers conclude in a recent paper.

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