An outbreak of a disease called monkeypox is currently taking place in many countries that do not typically have cases. This can be concerning, especially for people whose loved ones or community have been affected. Some cases have been identified through sexual health clinics in communities of gay, bisexual and other men who have sex with men.
It is important to note that the risk of monkeypox is not limited to men who have sex with men. Anyone who has close contact with someone who is infectious is at risk. However, given that the virus is being identified in these communities, learning about monkeypox will help ensure that as few people as possible are affected and that the outbreak can be stopped.
This public health advice contains information on how monkeypox spreads, what to do if you think you have symptoms and how to protect yourself and others. It can be used by community leaders, influencers, health workers and people attending social events and parties to inform and engage communities of men who have sex with men.
What you need to know
An outbreak of a disease called monkeypox is happening in some countries where the virus is not typically found. Some of these cases are being found in communities of gay, bisexual and other men who have sex with men. Transgender people and gender-diverse people may also be more vulnerable in the context of the current outbreak.
Symptoms include:
Rash with blisters on face, hands, feet, eyes, mouth and/or genitals
Fever
Swollen lymph nodes
Headaches
Muscle aches
Low energy
You can catch monkeypox if you have close physical contact with someone who is showing symptoms. This includes touching and being face-to-face.
Monkeypox can spread during close skin-to-skin contact during sex, including kissing, touching, oral and penetrative sex with someone who has symptoms. Avoid having close contact with anyone who has symptoms.
Protect yourself and others by:
Isolating at home and talking to a health worker if you have symptoms
Avoid skin-to-skin or face-to-face contact, including sexual contact with anyone who has symptoms
Clean hands, objects, and surfaces that have been touched regularly
Wear a mask if you are in close contact with someone with symptoms
The article is published courtesy of the World Health Organization (WHO).
A research team supported by the National Institutes of Health has identified characteristics of people with long COVID and those likely to have it.
Transmission electron micrograph of SARS-CoV-2 virus particles, isolated from a patient.NIAID
Scientists, using machine learning techniques, analyzed an unprecedented collection of electronic health records (EHRs) available for COVID-19 research to better identify who has long COVID. Exploring de-identified EHR data in the National COVID Cohort Collaborative (N3C), a national, centralized public database led by NIH’s National Center for Advancing Translational Sciences (NCATS), the team used the data to find more than 100,000 likely long COVID cases as of October 2021 (as of May 2022, the count is more than 200,000). The findings appear in The Lancet Digital Health.
Long COVID is marked by wide-ranging symptoms, including shortness of breath, fatigue, fever, headaches, “brain fog” and other neurological problems. Such symptoms can last for many months or longer after an initial COVID-19 diagnosis. One reason long COVID is difficult to identify is that many of its symptoms are similar to those of other diseases and conditions. A better characterization of long COVID could lead to improved diagnoses and new therapeutic approaches.
“It made sense to take advantage of modern data analysis tools and a unique big data resource like N3C, where many features of long COVID can be represented,” said co-author Emily Pfaff, Ph.D., a clinical informaticist at the University of North Carolina at Chapel Hill.
The N3C data enclave currently includes information representing more than 13 million people nationwide, including nearly 5 million COVID-19-positive cases. The resource enables rapid research on emerging questions about COVID-19 vaccines, therapies, risk factors and health outcomes.
The new research is part of a related, larger trans-NIH initiative, Researching COVID to Enhance Recovery (RECOVER), which aims to improve the understanding of the long-term effects of COVID-19, called post-acute sequelae of SARS-CoV-2 infection (PASC). RECOVER will accurately identify people with PASC and develop approaches for its prevention and treatment. The program also will answer critical research questions about the long-term effects of COVID through clinical trials, longitudinal observational studies, and more.
In the Lancet study, Pfaff, Melissa Haendel, Ph.D., at the University of Colorado Anschutz Medical Campus, and their colleagues examined patient demographics, health care use, diagnoses and medications in the health records of 97,995 adult COVID-19 patients in the N3C. They used this information, along with data on nearly 600 long COVID patients from three long COVID clinics, to create three machine learning models to identify long COVID patients.
In machine learning, scientists “train” computational methods to rapidly sift through large amounts of data to reveal new insights — in this case, about long COVID. The models looked for patterns in the data that could help researchers both understand patient characteristics and better identify individuals with the condition.
The models focused on identifying potential long COVID patients among three groups in the N3C database: All COVID-19 patients, patients hospitalized with COVID-19, and patients who had COVID-19 but were not hospitalized. The models proved to be accurate, as people identified as at risk for long COVID were similar to patients seen at long COVID clinics. The machine learning systems classified approximately 100,000 patients in the N3C database whose profiles were close matches to those with long COVID.
“Once you’re able to determine who has long COVID in a large database of people, you can begin to ask questions about those people,” said Josh Fessel, M.D., Ph.D., senior clinical advisor at NCATS and a scientific program lead in RECOVER. “Was there something different about those people before they developed long COVID? Did they have certain risk factors? Was there something about how they were treated during acute COVID that might have increased or decreased their risk for long COVID?”
The models searched for common features, including new medications, doctor visits and new symptoms, in patients with a positive COVID diagnosis who were at least 90 days out from their acute infection. The models identified patients as having long COVID if they went to a long COVID clinic or demonstrated long COVID symptoms and likely had the condition but hadn’t been diagnosed.
“We want to incorporate the new patterns we’re seeing with the diagnosis code for COVID and include it in our models to try to improve their performance,” said the University of Colorado’s Haendel. “The models can learn from a greater variety of patients and become more accurate. We hope we can use our long COVID patient classifier for clinical trial recruitment.”
Scientists at the National Institutes of Health have found that a process in cells may limit infectivity of SARS-CoV-2, and that mutations in the alpha and delta variants overcome this effect, potentially boosting the virus’s ability to spread. The findings were published online in the Proceedings of the National Academy of Sciences. The study was led by Kelly Ten Hagen, Ph.D., a senior investigator at NIH’s National Institute of Dental and Craniofacial Research (NIDCR).
Since the coronavirus pandemic began in early 2020, several more-infectious variants of SARS-CoV-2, the virus that causes COVID-19, have emerged. The original, or wild-type, virus was followed by the alpha variant, which became widespread in the United States in early 2021, and the delta variant, which is the most prevalent strain circulating today. The variants have acquired mutations that help them spread and infect people more easily. Many of the mutations affect the spike protein, which the virus uses to get into cells. Scientists have been trying to understand how these changes alter the virus’s function.
“Throughout the pandemic, NIDCR researchers have applied their expertise in the oral health sciences to answer key questions about COVID-19,” said NIDCR Director Rena D’Souza, D.D.S., Ph.D. “This study offers fresh insights into the greater infectivity of the alpha and delta variants and provides a framework for the development of future therapies.”
The outer surface of SARS-CoV-2 is decorated with spike proteins, which the virus uses to attach to and enter cells. Before this can happen, though, the spike protein must be activated by a series of cuts, or cleavages, by host proteins, starting with the furin enzyme. In the alpha and delta variants, mutations to the spike protein appear to enhance furin cleavage, which is thought to make the virus more effective at entering cells.
Studies have shown that in some cases protein cleavage can be decreased by the addition of bulky sugar molecules—a process carried out by enzymes called GALNTs—next to the cleavage site. Ten Hagen’s team wondered if this happens to the SARS-CoV-2 spike protein, and if so, whether it changes the protein’s function.
To find out, the scientists studied the effects of GALNT activity on spike protein in fruit fly and mammalian cells. The experiments showed that one enzyme, GALNT1, adds sugars to wild-type spike protein, and this activity reduces furin cleavage. By contrast, mutations to the spike protein, like those in the alpha and delta variants, decrease GALNT1 activity and increase furin cleavage. This suggested that GALNT1 activity may partially suppress furin cleavage in wild-type virus, and that the alpha and delta mutations overcome this effect, allowing furin cleavage to go unchecked.
Further experiments supported this idea. The researchers expressed either wild-type or mutated spike in cells grown in a dish. They observed the cells’ tendency to fuse with their neighbors, a behavior that may facilitate spread of the virus during infection. The scientists found that cells expressing mutated spike protein fused with neighbors more often than cells with the wild-type version. Cells with wild-type spike also fused less in the presence of GALNT1, suggesting that its activity may limit spike protein function.
“Our findings indicate that the alpha and delta mutations overcome the dampening effect of GALNT1 activity, which may enhance the virus’s ability to get into cells,” said Ten Hagen.
To see if this process might also occur in people, the team analyzed RNA expression in cells from healthy volunteers. The researchers found wide expression of GALNT1 in lower and upper respiratory tract cells that are susceptible to SARS-CoV-2 infection, indicating that the enzyme could influence infection in humans. The scientists theorized that individual differences in GALNT1 expression could affect viral spread.
“This study suggests that GALNT1 activity may modulate viral infectivity and provides insight into how mutations in the alpha and delta variants may influence this,” Ten Hagen said. The knowledge could inform future efforts to develop new interventions.
This research was supported by the NIDCR Division of Intramural Research. Support also came from the intramural program of the National Institute of Environmental Health Sciences.
The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, has awarded approximately $36.3 million to three academic institutions to conduct research to develop vaccines to protect against multiple types of coronaviruses and viral variants. The awards are intended to fuel vaccine research for a diverse family of coronaviruses, with a primary focus on potential pandemic-causing coronaviruses, such as SARS-CoV-2.
“The available COVID-19 vaccines have proven to be remarkably effective at protecting against severe disease and death,” said NIAID Director Anthony S. Fauci, M.D. “These new awards are designed to look ahead and prepare for the next generation of coronaviruses with pandemic potential.”
The new awards are funded by NIAID’s Division of Microbiology and Infectious Diseases and its Division of Allergy, Immunology, and Transplantation through the Emergency Awards Notice of Special Interest (NOSI) on Pa.n-Coronavirus Vaccine Development Program Projects. The notice was issued in November 2020 while many SARS-CoV-2 vaccines were still under development because a critical need remained for prophylactic vaccines offering broad protective immunity against other coronaviruses, such as Middle East Respiratory Syndrome Coronavirus (MERS-CoV) and Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV).
The awards are designed to fund multidisciplinary teams at each institution to conduct research focused on incorporating understanding of coronavirus virology and immunology, immunogen design, and innovative vaccine and adjuvant platforms and technologies to discover, design, and develop pan-coronavirus vaccine candidates that provide broad protective immunity to multiple coronavirus strains. Specific programs will address coronavirus diversity and infectious potential in humans, include innovative immunogen design and vaccine platforms, and approaches to elicit potent and durable pan-coronavirus immunity, and evaluate vaccine candidates in preclinical models. The awardees are expected to be flexible in the response to emerging knowledge about SARS-CoV-2 immune responses and infection and factor in new information as vaccines candidates are developed. Additional awards are expected to be issued under the NOSI in 2022 to support pan-coronavirus vaccine research at more institutions.
The new awards build on the $1.2 billion investment NIAID has made in coronavirus vaccine research since the COVID-19 pandemic began, including multiple projects in pan-coronavirus vaccine research in the NIAID intramural and extramural programs.
A key goal of the initiative is to develop multivalent vaccine platforms and strategies suitable for use in vulnerable populations and to understand vaccine-induced responses and efficacy related to a person’s age or sex.
COVID-19 poses major challenges to population health and well-being globally and hinders progress in meeting the SDGs and WHO’s Triple Billion targets.
The WHO Triple Billion targets are a shared vision among WHO and Member States, which help countries to accelerate the delivery of the SDGs. By 2023 they aim to achieve: one billion more people enjoying better health and well-being, one billion more people benefiting from universal health coverage (covered by health services without experiencing financial hardship) and one billion more people better protected from health emergencies.
As of 1 May 2021, over 153 million confirmed COVID-19 cases and 3.2 million related deaths have been reported to WHO. The Region of the Americas and the European Region have been the most affected, together comprising over three quarters of cases reported globally, with respective case rates per 100 000 population of 6114 and 5562 and almost half (48%) of all reported COVID-19-associated deaths occurring in the Region of the Americas, and one third (34%) in the European Region.
COVID-19 has surfaced long-standing inequalities across income groups, disrupted access to essential medicines and health services, stretched the capacity of the global health workforce and revealed significant gaps in country health information systems.
While high-resource settings have faced challenges related to overload in the capacity of health services, the pandemic poses critical challenges to weak health systems in low-resource settings and is jeopardising hard-won health and development gains made in recent decades.
Data from 35 high-income countries shows that preventive behaviours decrease as household overcrowding (a measure of socioeconomic status) increases.
Overall, 79% (median value of 35 countries) of people living in uncrowded households reported trying to physically distance themselves from others compared to 65% in extremely overcrowded households. Regular daily handwashing practices (washing hands with soap and water or using hand sanitizers) were also more common among people who lived in uncrowded households (93%) compared to those living in extremely overcrowded households (82%). In terms of mask-wearing in public, 87% of people living in uncrowded households wore a mask all or most of the time when in public in the last seven days compared to 74% of people living in extremely overcrowded conditions.
The combination of conditions related to poverty reduce access to health services and evidence-based information while increasing risky behaviours.
SARS-CoV-2 is the virus that causes COVID-19. MK-4482, delivered orally, is now in human clinical trials. Remdesivir, an antiviral drug already approved by the U.S. Food and Drug Administration for use against COVID-19, must be provided intravenously, making its use primarily limited to clinical settings.
In their study, published in the journal Nature Communications, the scientists found MK-4482 treatment effective when provided up to 12 hours before or 12 hours after infecting the hamsters with SARS-CoV-2. These data suggest that MK-4482 treatment potentially could mitigate high-risk exposures to SARS-CoV-2, and might be used to treat established SARS-CoV-2 infection alone or possibly in combination with other agents.
The same research group, located at Rocky Mountain Laboratories, part of NIH’s National Institute of Allergy and Infectious Diseases in Hamilton, Montana, developed the hamster model last year to mimic SARS-CoV-2 infection and mild disease in people. The University of Plymouth in the United Kingdom collaborated on these most recent studies.
The project involved three groups of hamsters: a pre-infection treatment group; a post-infection treatment group; and an untreated control group. For the two treatment groups, scientists administered MK-4482 orally every 12 hours for three days. At the conclusion of the study, the animals in each of the treatment groups had 100 times less infectious virus in their lungs than the control group. Animals in the two treatment groups also had significantly fewer lesions in the lungs than the control group.
The scientists determined the MK-4482 treatment doses for this study based on previous experiments performed in mouse models of SARS-CoV-1 and MERS-CoV. In those studies, MK-4482 was effective at stopping the viruses from replicating.
With funding support from NIAID, Emory University’s Drug Innovation Ventures group in Atlanta developed MK-4482 (also known as molnupiravir and EIDD-2801) to treat influenza. Merck and Ridgeback Biotherapeutics are now jointly developing and evaluating MK-4482 as a potential COVID-19 treatment. The drug is in Phase 2 and 3 human clinical studies.
A single dose of an experimental COVID-19 vaccine delivered into the nose of rhesus macaques protected their lungs and nasal region from SARS-CoV-2 infection, a new study from National Institutes of Health scientists and colleagues shows.
The vaccine, known in its pre-clinical formulation as ChAd-SARS-CoV-2-S, is undergoing clinical trials in India under the name BBV154.
Scientists at Washington University School of Medicine in St. Louis developed ChAd-SARS-CoV-2-S, which is designed similarly to AZD1222—a COVID-19 vaccine developed by the University of Oxford and pharmaceutical company AstraZeneca, both based in the United Kingdom.
AZD1222 has been authorized for use in parts of the world. Both vaccines use an adenoviral vector that infects chimpanzees to deliver the genetic information for an immune-stimulating protein from SARS-CoV-2, the virus that causes COVID-19. ChAd-SARS-CoV-2-S is based on a different strain of chimp adenovirus than AZD1222 and delivers the genetic information to produce a stabilized form of the spike protein, which is found on the surface of SARS-CoV-2.
The Washington University scientists successfully tested the protective efficacy of ChAd-SARS-CoV-2-S against SARS-CoV-2 in mice and hamsters. They then collaborated for the macaque study, published in Cell Reports Medicine, with colleagues at NIH’s National Institute of Allergy and Infectious Diseases (NIAID).
In work completed at NIAID’s Rocky Mountain Laboratories in Hamilton, Montana, scientists immunized six macaques with ChAd-SARS-CoV-2-S and six with an inactive control; the immunization was delivered into the nose. Three weeks later, scientists detected protective antibodies against SARS-CoV-2 in animals vaccinated with ChAd-SARS-CoV-2-S, but not in the control animals. Four weeks after immunization, scientists exposed all 12 animals to high doses of SARS-CoV-2 delivered to the nose and trachea. Throughout the following week scientists checked animals for disease, virus growth in the lung and virus transmission from the nose. The overall data shows that ChAd-SARS-CoV-2-S protected the upper and lower respiratory tracts of the vaccinated animals from disease and virus transmission compared to the control animals.
ChAd-SARS-CoV-2-S is licensed in India to Bharat Biotech as BBV154. In the United States and Europe, Precision Virologics, Inc., holds the license for the investigational vaccine.
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