Discovery of antibody structure could lead to treatment for Crimean Congo Hemorrhagic Fever virus

Scott D. Pegan, a professor of biomedical sciences
Photo Source: University of California, Riverside

A research team led by the University of California, Riverside, has discovered important details about how therapeutically relevant human monoclonal antibodies can protect against Crimean Congo Hemorrhagic Fever virus, or CCHFV. Their work, which appears online in the journal Nature Communications, could lead to the development of targeted therapeutics for infected patients.

An emerging zoonotic disease with a propensity to spread, CCHF is considered a priority pathogen by the World Health Organization, or WHO. CCHF outbreaks have a mortality rate of up to 40%. Originally described in Crimea in 1944–1945, and decades later in the Congo, the virus has recently spread to Western Europe through ticks carried by migratory birds. The disease is already endemic in Africa, the Balkans, the Middle East, and some Asian countries. CCHFV is designated as a biosafety level 4 pathogen (the highest level of biocontainment) and is a Category A bioterrorism/biological warfare agent. There is no vaccine to help prevent infection and therapeutics are lacking.

Scott D. Pegan, a professor of biomedical sciences in the UCR School of Medicine, collaborated on this study with the United States Army Medical Research Institute of Infectious Diseases, or USAMRIID, which studies CCHFV because of the threat it poses to military personnel around the world. They examined monoclonal antibodies, or mAbs, which are proteins that bind to antigens — foreign substances that enter the body and cause the immune system to mount a protective response.

In a previous publication, USAMRIID scientists Joseph W. Golden and Aura R. Garrison reported that an antibody called 13G8 protected mice from lethal CCHFV when administered post-infection. They provided Pegan with the sequence information for that antibody, clearing the way for UCR to “humanize” it and conduct further research.

Blood group can predict risk of contracting viral disease

People with blood type Rh(D) have a higher risk of being infected by parvovirus
Photo Credit: Bartek Kopała

The risk of being infected by parvovirus is elevated in those people who have blood group Rh(D), according to a study published in The Journal of Infectious Diseases by researchers from Karolinska Institutet in collaboration with Octapharma.  

Fifth disease is a viral disease caused by parvovirus. Most often, school-age children are affected with common symptoms such as red blotches on the cheeks that can also spread to the arms and legs. Even adults can become infected, but many do not show any symptoms.  

In a new study, researchers can now demonstrate that the risk of contracting the disease is elevated if the person belongs to the blood group Rhesus D antigen or what is called Rh(D). In addition to the blood typing in the AB0 system, the Rh system is the most common.

SARS-CoV-2 detection in 30 minutes using gene scissors

Multiplex chip of a Freiburg research team: On this chip, the viral load in the nasal swab and, if necessary, the antibiotic concentration in the blood of COVID-19 patients could be measured simultaneously.
Photo Credit: AG Disposable Microsystems/University of Freiburg

Researchers of the University of Freiburg introduce biosensor for the nucleic acid amplification-free detection of SARS-CoV-2 RNA

CRISPR-Cas is versatile: Besides the controversial genetically modified organisms (GMOs), created through gene editing, various new scientific studies use different orthologues of the effector protein ‘Cas’ to detect nucleic acids such as DNA or RNA.

In its most recent study, the research group headed by microsystems engineer Dr. Can Dincer of the Department of Microsystems2 Engineering, University of Freiburg introduces a microfluidic multiplexed chip for the simultaneous measurement of the viral load in nasal swabs and (if applicable) the blood antibiotic levels of COVID-19 patients.

Rapid test or PCR?

The market launch of rapid antigen test kits has significantly changed the way in which society handles the effects of the pandemic: Individuals suspecting an infection with SARS-CoV-2 can now test themselves at home with kits that are readily available at most drug stores, pharmacies and supermarkets, instead of making an, oftentimes difficult to acquire, appointment for PCR testing, that requires 1 to 3 additional days to receive the result. This convenience is, however, paid for with test sensitivity. This issue became flagrantly apparent during the wave of infections last winter, when the ‘lateral flow devices’ frequently failed to detect infections with the Omicron-variant until after the onset of symptoms. “The trade-off between sensitivity and sample-to-result time could potentially be bridged using our method,” says Midori Johnston, first author of the study, that is now being published in the journal Materials Today.

Pocket feature shared by deadly coronaviruses could lead to pan-coronavirus antiviral treatment

Spike glycoprotein structure of SARS-CoV, the coronavirus causing the 2002 outbreak. When linoleic acid is bound, the structure is locked in a non-infectious form. The cryo-EM density, calculated by cloud computing, is shown (left) along with the protein structure (middle). Linoleic acid molecules are colored orange. A zoom-in of the pocket (boxed), conserved in all deadly coronaviruses, is shown
 Illustration Credit: Christiane Schaffitzel and Christine Toelzer, University of Bristol

Scientists have discovered why some coronaviruses are more likely to cause severe disease, which has remained a mystery, until now. Researchers of the University of Bristol-led study, published in Science Advances today [23 November], say their findings could lead to the development of a pan-coronavirus treatment to defeat all coronaviruses—from the 2002 SARS-CoV outbreak to Omicron, the current variant of SARS-CoV-2, as well as dangerous variants that may emerge in future.

In this new study, an international team, led by Bristol's Professor Christiane Schaffitzel, scrutinized the spike glycoproteins decorating all coronaviruses. They reveal that a tailor-made pocket feature in the SARS-CoV-2 spike protein, first discovered in 2020, is present in all deadly coronaviruses, including MERS and Omicron. In striking contrast, the pocket feature is not present in coronaviruses which cause mild infection with cold-like symptoms.

The team say their findings suggest that the pocket, which binds a small molecule, linoleic acid—an essential fatty acid indispensable for many cellular functions including inflammation and maintaining cell membranes in the lungs so that we can breathe properly—could now be exploited to treat all deadly coronaviruses, at the same time rendering them vulnerable to a linoleic acid-based treatment targeting this pocket.

New Omicron subvariant BQ.1.1 resistant to all therapeutic antibodies

The Omicron subvariants BA.1, BA.4, BA.5 as well as Q.1.1 have a high number of mutations in the spike protein. Some of these mutations are escape mutations that allow the virus to escape neutralization by antibodies. In addition, resistance to biotechnologically produced antibodies, which are administered to high-risk patients as a preventive measure or as therapy for a diagnosed SARS-CoV-2 infection, is also developing. Omicron sub-lineage BQ.1.1 is the first variant resistant to all antibody therapies currently approved by the EMA (European Medicines Agency) and/or FDA (US Food and Drug Administration).
Figure Credit: Markus Hoffmann, German Primate Center – Leibniz Institute for Primate Research.

Are the currently approved antibody therapies used to treat individuals at increased risk for severe COVID-19 disease also effective against currently circulating viral variants? A recent study by researchers at the German Primate Center (DPZ) – Leibniz Institute for Primate Research and Friedrich-Alexander University Erlangen-Nürnberg shows that the Omicron sub-lineage BQ.1.1, currently on the rise worldwide, is resistant to all approved antibody therapies. published in the journal Lancet Infectious Diseases.

A growing trend of antibody evasion by new omicron subvariants

Scanning electron micrograph of a cell (purple) infected with the omicron strain of SARS-CoV-2 virus particles (orange), isolated from a patient sample and colorized.
Image Credit: NIAID/NIH

Three currently circulating omicron subvariants of SARS-CoV-2 – including two that currently make up almost 50% of reported COVID-19 infections in the U.S. – are better at evading vaccine- and infection-generated neutralizing antibodies than earlier versions of omicron, new research suggests.

Scientists tested neutralizing antibodies in blood serum samples from vaccinated and once-boosted or recently infected health care professionals against several subvariants in circulation. Three subvariants stood out for their resistance to the antibody immune response: BQ.1, BQ.1.1 and BA.2.75.2.

BQ.1 and BQ.1.1 are subvariants of the BA.4/5 omicron variants that have been dominating the last few months in the U.S., and each now accounts for about a quarter of current infections, according to the Centers for Disease Control and Prevention (CDC). BA.2.75.2, a mutant of the BA.2 omicron variant, was the best of all variants tested at evading neutralizing antibodies, but currently accounts for only a very small proportion of reported illnesses in the United States.

“In general, the subvariants BQ.1 and BQ.1.1 are much better compared to prior variants at evading the booster-mediated antibody response – the neutralizing antibody titers are clearly much lower. And those two variants are becoming dominant,” said Shan-Lu Liu, senior author the study and a virology professor in the Department of Veterinary Biosciences at The Ohio State University.

Covid-19: the Spike protein is no longer the only target

Possible mechanism of action of a drug targeting Nsp1 of SARS-CoV-2. In infected cells, Nsp1 blocks the ribosome mRNA canal by acting as a "cap" that prevents the expression of the host's mRNA. Linking a ligand to the proposed cryptic pocket highlighted in purple could prevent blockage mediated by Nsp1 and, ultimately, restore the ability of the ribosome to initiate the translation of the mRNA.
Photo Credit: UNIGE Alberto Borsatto

A research team led by the UNIGE reveals a hidden cavity on a key SARS-CoV-2 protein to which drugs could bind.

With the continuous emergence of new variants and the risk of new strains of the virus, the development of innovative therapies against SARS-CoV-2 remains a major public health challenge. Currently, the proteins that are on the surface of the virus and/or are involved in its replication are the preferred therapeutic targets, like the Spike protein targeted by vaccines. One of them, the non-structural protein Nsp1, had been studied little until now. A team from the University of Geneva (UNIGE), in collaboration with University College London (UCL) and the University of Barcelona, has now revealed the existence of a hidden ''pocket’ on its surface. A potential drug target, this cavity opens the way to the development of new treatments against Covid-19 and other coronaviruses. These results can be found in the journal eLife.

To prevent next pandemic research suggests we need to restore wildlife habit

Researchers found that bats disrupted by a lack of habitat and food move near humans in agricultural and urban areas, where they can spread Hendra virus to horses and then people.
Photo Credit: Vlad Kutepov

Preserving and restoring natural habitats in specific locations could prevent pathogens that originate in wildlife from spilling over into domesticated animals and humans, according to new research led by an international team of researchers, including Penn State.

The research, undertaken in Australia, found that when bats experience a loss of winter habitat and food shortages in their natural settings, their populations splinter and they excrete more virus. Bats disrupted by the lack of food move near humans in agricultural and urban areas. The team studied Hendra virus, a lethal virus that spills over from fruit bats to horses and then infects people.

“One of the biggest challenges we face are threats arising from bat-borne viruses that spillover into humans and have the potential to cause pandemics. Ebola, MERS, SARS, SARS-CoV-2, Nipah and Hendra are all good examples of this,” said Peter Hudson, Willaman Professor of Biology, Penn State. “The response to the pandemic has been to find ways to speed up vaccine development, but since infections invariably spread much faster than vaccine rollout, this reactive response will never stop a pandemic. Instead, the solution lies with preventing viral spillover from bats to humans.”

Call it a CRISPR conundrum

Model grass Brachypodium distachyon plant grown on liquid media.
Photo courtesy of Marta Torres, m-CAFEs postdoctoral researcher, Deutschbauer lab, Environmental Genomics and Systems Biology "
Credit: University of California, Lawrence Berkeley National Laboratory."

Bacteria use CRISPR-Cas systems as adaptive immune systems to withstand attacks from enemies like viruses. These systems have been adapted by scientists to remove or cut and replace specific genetic code sequences in a variety of organisms.

But in a new study, North Carolina State University researchers show that viruses engineered with a CRISPR-Cas system can thwart bacterial defenses and make selective changes to a targeted bacterium – even when other bacteria are in close proximity.

“Viruses are very good at delivering payloads. Here, we use a bacterial virus, a bacteriophage, to deliver CRISPR to bacteria, which is ironic because bacteria normally use CRISPR to kill viruses,” said Rodolphe Barrangou, the Todd R. Klaenhammer Distinguished Professor of Food, Bioprocessing and Nutrition Sciences at NC State and corresponding author of a paper describing the research published today in Proceedings of the National Academy of Sciences. “The virus in this case targets E. coli by delivering DNA to it. It’s like using a virus as a syringe.”

The NC State researchers deployed two different engineered bacteriophages to deliver CRISPR-Cas payloads for targeted editing of E. coli, first in a test tube and then within a synthetic soil environment created to mimic soil – a complex environment that can harbor many types of bacteria.

Limiting antibiotics for cows may create a new dairy market

Photo Credit: David Mark

Consumers would be willing to buy milk from cows only treated with antibiotics when medically necessary – as long as the price isn’t much higher than conventional milk, according to researchers at the College of Veterinary Medicine.

The findings suggest conventional farmers could tap a potentially large market for this type of milk if they can find the right price point – and that dairy consumers can help slow the rise of antimicrobial resistance.

“Most of the antibiotics produced throughout the world are used for animal agriculture. Therefore, reducing antibiotic use in animals, including dairy cattle, is necessary to tackle antibiotic resistance at a global scale,” said Dr. Renata Ivanek, professor in the Department of Population Medicine and Diagnostic Sciences. She is senior author on the study, which was published Nov. 4 in the Journal of Dairy Science.

In the paper, the researchers propose a new label for milk that indicates responsible antibiotic use (RAU), which would leverage consumer preferences to reduce the use of antibiotics on commercial dairy farms. The study showed that, although a consumer’s willingness to pay for the RAU-labeled milk was comparable to how much they would pay for the unlabeled milk, they strongly preferred the RAU-labeled milk over the unlabeled milk option. Therefore, the researchers hypothesize this new RAU label would entice farmers to minimize antibiotics more than they do for conventional, unlabeled milk.

Therapeutic HIV vaccine with Oxford technology achieves encouraging results

Artist illustration of the HIV virus.
Illustration Credit: Darwin Laganzon

A phase I/IIa clinical trial that the University of Oxford collaborated on has demonstrated that a T-cell therapeutic HIV vaccine was associated with better control of the virus rebound when antiretroviral therapy (ART) was temporarily withdrawn.

Researchers carrying out the AELIX-002 study, whose results have been published in Nature Medicine, reported that two fifths of participants without any genetic background associated with spontaneous HIV control were able to stay off ART for the six-month duration of the supervised ART pause.

The vaccine in the study – developed by AELIX Therapeutics – delivered the HIVACAT T-cell Immunogen (HTI) using a combination of DNA vector, modified vaccinia virus Ankara (MVA) vector and simian adenovirus vector ChAdOx1. The latter two vaccines were constructed at Oxford.

Tomáš Hanke, Professor of Vaccine Immunology at the Jenner Institute, Nuffield Department of Medicine, who leads on HIV vaccine development, said:

‘This result provides further encouragement that active immunization against HIV may be possible, slowing HIV replication, providing a window of treatment holidays for people living with HIV and eventually leading to HIV cure. T cells/T-cell vaccines are likely to play an important part in the final package for HIV cure and, perhaps, other advanced therapies for difficult diseases.’

Infants are less likely to contract COVID, develop severe symptoms than other household caregivers

Image by Pexels

Infants whose mothers test positive for COVID-19 tend to develop less-severe symptoms than their parents, if they become infected with the virus at all.

In one of the first studies to explore how COVID-19 specifically affects older infants, researchers from the University of Washington and at institutions at four other locations in the Western and Southern U.S. found that the number of infected people in a household was the factor most closely linked with the infant’s likelihood of being infected.

“The focus on infants early in the pandemic was about possible transmission risks during pregnancy, birth or through breastfeeding, but there were other questions about the risks in the household to infants and other children when caregivers are sick,” said Melanie Martin, assistant professor of anthropology at the UW and the first author of the study, which in the journal Frontiers in Immunology. “Infants are in the most contact, and very close contact, with their caregiver than with any other family members. And so, we asked, "How much are infants at risk, and how do you protect children when they are sick?”

The study analyzed surveys and antibody results (taken from pin-prick blood samples) of 46 pairs of COVID-positive mothers and their infants for two months following maternal infection. Infants were at least 1 month old, and COVID-positive mothers were enrolled in the study within days, sometimes hours, of receiving their positive PCR test results. The researchers also recruited a comparative group of 11 COVID-negative mothers, who tested negative after exposure or symptoms, and a control group of 26 mothers with no known COVID exposures or symptoms.

Viruses can ‘hitchhike’ on microplastics

Photo Credit: Naja Bertolt Jensen

Microplastics are not just tiny particles that can be ingested, they can also carry viruses, a University of Queensland study has revealed.

The study, led by Associate Prof Jianhua Guo and Dr Ji Lu from UQ’s Australian Centre for Water and Environmental Biotechnology (ACWEB), investigated if microplastics have the ability to harbor viruses, including the one found inside E. coli bacteria.

“We often hear about the human and environmental harm caused by microplastics in water, but there is little known about whether the tiny microplastic particles can carry viruses,” Dr Guo said.

“What we found is that viruses can hitchhike on microplastics and prolong their infectivity, which means there could be an increased risk of virus transmission throughout waterways and the environment.”

Dr Lu said they used the E. coli bacteriophage in the study, which is a virus that infects and replicates within the bacteria itself and is not harmful to humans.

Study Identifies Key T Cells for Immunity Against Fungal Pneumonia

 GM-CSF+ and IL-17A+ lineages of T cells are instrumental in controlling many fungal and bacterial infections and implicated in autoimmune pathology. This study shows that GM-CSF expressing Tc17 cells are necessary for mediating fungal vaccine immunity without augmenting pathology.
Credit: Som Nanjappa

Researchers at the University of Illinois College of Veterinary Medicine have demonstrated in a mouse model that a specific type of T cell, one of the body’s potent immune defenses, produces cytokines that are necessary for the body to acquire immunity against fungal pathogens. This finding could be instrumental in developing novel, effective fungal vaccines.

Despite vaccines being hailed as one of the greatest achievements of medicine, responsible for controlling or eradicating numerous life-threatening infectious diseases, no vaccines have been licensed to prevent or control human fungal infections.

This lack proved especially deadly during the COVID-19 pandemic. In countries where steroids were widely used to suppress inflammation of the lungs, COVID-19 patients with preexisting conditions such as uncontrolled diabetes showed a greater likelihood of developing lethal fungal infections.

Covid-19 is linked to increased degradation of connections between nerve cells in a new brain model

Postdoctoral fellow Samudyata and doctoral student Susmita Malwade.
Source: Karolinska Institutet

Researchers at Karolinska Institutet have used cellular reprogramming in a new study to create human three-dimensional brain models and infected them with SARS-CoV-2. In infected models, the brain's immune cells showed an excessive elimination of connections between the nerve cells. The gene expression of these cells also mimicked changes observed in neurodegenerative diseases. The results hope to identify new treatments for cognitive symptoms after Covid-19 infection.

Several studies have reported persistent cognitive symptoms following a covid-19 infection, but the underlying mechanisms for this are still unknown. The researchers behind the study, published in the journal Molecular Psychiatry, have created from human induced pluripotent stem cells (iPS) three-dimensional models of the brain in test tubes, so-called brain organoids. The model differs from previous organoid models in that they also contain microglia - the brain's immune cells. In the infected models, microglia regulated genes involved in phagocytosis, "cell-eating," the researchers could also see how microglia contained an increased amount of proteins from brain cell connections, so-called synapses. The developed model and results of the study can help guide future efforts to address cognitive symptoms in the aftermath of COVID-19 and other neuroinvasive viral infections.

Attack on 2 fronts leads ocean bacteria to require carbon boost

The study is the first to observe these complex interactions under the ocean surface: photosynthetic bacteria simultaneously infected with viruses and floating in the presence of organisms, called protists, that eat them. Photo Credit: Matt Hardy

The types of ocean bacteria known to absorb carbon dioxide from the air require more energy – in the form of carbon – and other resources when they’re simultaneously infected by viruses and face attack from nearby predators.

Viruses are abundant in the ocean, and research now suggests that marine viruses have beneficial functions, including helping to drive carbon absorbed from the atmosphere to permanent storage on the ocean floor. When viruses infect other microbes in that environment (and anywhere, in fact), the interaction results in creation of entirely new organisms called “virocells.”

In this new study, researchers worked with cyanovirocells – cyanobacteria that absorb carbon and release oxygen through photosynthesis that have been infected with viruses. The analysis of changes in the infected bacteria’s gene activation and metabolism under lab conditions designed to mimic nature hints at an intriguing possibility: The dual threat of viral infection and drifting among hungry predator microbes might lead cyanovirocells to take in more carbon.

Obesity and biological sex may make individuals more vulnerable to COVID-19

A new West Virginia University study suggests obesity may impair the ability to fight off SARS-CoV-2, the virus that causes COVID-19, in a sex-dependent manner.
Credit: WVU Illustration/Graham Curry

A new animal study from Katherine Lee, a researcher with the West Virginia University School of Medicine, investigates why individuals with obesity may have a particularly difficult time fending off SARS-CoV-2, the virus that causes COVID-19. Specifically, female obese mice experienced worse disease symptoms, showing the importance of both obesity and biological sex in COVID-19 outcomes.

Lee’s findings appear in the journal iScience.

Obesity dramatically increases someone’s risk of being hospitalized, placed on a ventilator or dying due to COVID-19. Considering that about two out of every five Americans are obese, that risk is far from negligible.

“No human is 100% healthy in every respect,” said Lee, a doctoral student in the Department of Microbiology, Immunology and Cell Biology. “There are always going to be little differences in the way our bodies function and those changes can ultimately affect the ways we respond to everything. So, I think as soon as we start incorporating those differences and changes — metabolic diseases and preexisting conditions — into our work, we can learn more about how vaccines and therapeutics might be more or less effective in these people.”

Virologists close gap on unknown viruses affecting amphibians and reptiles

It took three years to identify the virus that all but wiped out the Bellinger River turtle in 2015. It is hoped that amassing new viral data affecting herptiles will allow quicker conservation responses.
Credit: Pelagic, CC BY-SA 4.0

New knowledge about amphibian and reptile viruses will help us act faster to conserve threatened species.

A study of viruses that affect amphibians and reptiles has closed the gap on the knowledge of viruses affecting animals which until now has largely focused on humans and other mammals.

Third year PhD student Emma Harding, who led the study published today in ISME Communications, used the UNSW supercomputer Katana to comb through petabytes (millions of gigabytes) of publicly available amphibian and reptile RNA data in search of new viruses affecting these classes of animals.

“We know a lot about viruses that infect us and livestock, however not many people have investigated viruses that infect amphibians and reptiles, even though there are over 18,000 species globally,” Ms. Harding, lead author on the paper, says.

“We looked through more than 200 RNA datasets from amphibians and reptiles for evidence of new viruses that could lead to disease. We found 26 new viruses from a range of different families and now have a better understanding of what viruses can infect these animals.”

The cell sentinel that neutralizes hepatitis B

Confocal microscopy images showing in the cell nucleus (blue), the recruitment of Smc5/6 (green) by SLF2 (red) into PML bodies.
Credit: UNIGE - Laboratory of Professor Michel Strubin - Regulation of hepatitis B virus gene expression - Department of Microbiology and Molecular Medicine.

The hepatitis B virus (HBV) is responsible for one of the most serious and common infectious diseases. Transmitted through biological fluids, it attacks the liver cells. The chronic form of the disease can lead to serious complications, including cirrhosis and liver cancer. There is no effective treatment for the chronic form of the disease, which can only be prevented by vaccination. After identifying a key protein complex that is active when our body is infected by the virus, a team from the University of Geneva (UNIGE) has deciphered the precise functioning of this protective mechanism, opening the way to new therapeutic targets. These results can be read in the journal Nature Structural and Molecular Biology.

Hepatitis B is the most common form of hepatitis. It is a viral disease caused by the hepatitis B virus. It is mainly blood or sexually transmitted. It is up to 100 times more contagious than HIV. By infecting the liver cells, this virus causes a transitory inflammation of this organ that can also evolve towards a chronic infection. This can then lead to serious pathologies, such as cirrhosis or liver cancer. It is estimated that nearly one million people die each year from this disease worldwide. There is no definitive treatment for chronic hepatitis B. The only way to prevent it is to be vaccinated before the disease appears.

In 2016, a UNIGE team led by Michel Strubin, an associate professor in the Department of Microbiology and Molecular Medicine and in the Geneva Centre for Inflammation Research at the UNIGE Faculty of Medicine, revealed a mechanism that is crucial for understanding this disease: when our immune system defends itself against it, a complex - i.e. an interdependent set - of six proteins called SMC5/6, present in our cells, detects the viral DNA and blocks it. The virus then strikes back and produces a specific protein, the X protein. This protein enters the cell and degrades SMC5/6, which is no longer able to play its sentinel role.

Coronavirus formation is successfully modeled

Roya Zandi (left) and Siyu Li. (UCR/Zandi lab)
Source: University of California, Riverside

A physicist at the University of California, Riverside, and her former graduate student have successfully modeled the formation of SARS-CoV-2, the virus that spreads COVID-19, for the first time.

In a paper published in Viruses, a journal, Roya Zandi, a professor of physics and astronomy at UCR, and Siyu Li, a postdoctoral researcher at Songshan Lake Materials Laboratory in China, offer an overall understanding of the assembly and formation of SARS-CoV-2 from its constituent components.

“Understanding viral assembly has always been a key step leading to therapeutic strategies,” Zandi said. “Numerous experiments and simulations of viruses such as HIV and hepatitis B virus have had a remarkable impact on elucidating their assembly and providing means to combat them. Even the simplest questions regarding the formation of SARS-CoV-2 remain unanswered.”

Zandi explained that a critical step in the life cycle of any virus is the packaging of its genome into new virions or virus particles. This is an especially challenging task for coronaviruses, like SARS-CoV-2, with their very large RNA genomes. Indeed, coronaviruses have the largest genome known for a virus that uses RNA as its genetic material.