SARS-CoV-2 Salivary Tests

The benefits of saliva sampling for frequent and massive COVID-19 testing

Saliva tests for detection of SARS-CoV-2 RNA and antigens are becoming widely available lately. What are the advantages and disadvantages of sampling saliva over the nasal swabs? Saliva sampling simply involves spitting into a collection container. Recently, the U.S. Food and Drug Administration (FDA) also authorized the first diagnostic test with the option of home-collected saliva samples by using the Spectrum Solutions LLC SDNA-1000 Saliva Collection Device. The collected samples are then sent to a lab for further processing and analysis. Therefore, saliva sampling is much simpler and less uncomfortable than nasal swab sampling. This makes taking a sample at home or point of care much easier and more practical. It does not require collection by trained and protected medical personnel wearing personal protective equipment, thus reducing a considerable risk to healthcare workers. In contrast to nasal swab sampling, this approach is not affected by global shortages of swabs and personal protective equipment. In general, saliva sampling should permit more widespread and frequent testing. It is, of course, important that the test be as reliable and sensitive as the nasal swab test, but these appear to be reasonably similar [(1-3).

The current gold standard for COVID-19 diagnosis is real-time reverse transcription polymerase chain reaction (RT-PCR) detection of SARS-CoV-2 from collected samples. Concomitant with the advent of saliva sampling, techniques to simplify the detection of viral RNA have been introduced by eliminating the need for specific equipment, thermal cyclers. This makes it far more adaptable in resource poor settings, which often don’t have the relatively expensive PCR thermal cyclers. One such technique is reverse transcription loop-mediated isothermal amplification (RT-LAMP), which has been previously used to detect other viruses, including Zika and Ebola. A typical RT-LAMP assay takes place at a constant 63°C and the presence of viral RNA generates a color change in as little as a half an hour. A recent modification of the technique that uses inhibitors of salivary RNAs has been claimed to detect a single copy of viral RNA. These methods are obviously not specific to saliva tests, but use of saliva samples should facilitate a mass testing of SARS-CoV-2.

Several new developments in testing for viral RNA combine LAMP isothermal amplification with a technique called lateral flow, in which amplified samples are applied to a strip and allowed to flow along the strip. Amplified viral cDNA is detected by application of a CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)-CAS12 complex designed to bind to a specific viral sequence. When the CRISPR-CAS12 complex finds and binds its target, it releases a chromophore, which is visualized directly or fluorescently as a specific band on the strip. The CRISPR-CAS12 DETECTR is claimed to have a sensitivity of 95% and specificity of 100% compared to the CDC RT-PCR test (4) despite a concern of false negative results. In addition, STOP (SHERLOCK Testing in One Pot) uses similar technology. STOP has a detection limit of 100 viral RNA copies. Results from both tests are obtained in an hour or less, and analyses of the strips are obviously simple. Positive results are indicated by an exhibition of specific band on the strip.

Of course, all these tests, even though they can use point of care collection, require analyses in laboratories. A true point of care test would be one that could be used without need for laboratory involvement, similar to home pregnancy tests. Several of these kinds of tests are in development. For example, a test would involve placing a drop of saliva onto a device, the size of a quarter, and plugging it in to a smart phone. DNA aptamers on the device bind to viral proteins and then are detected by voltage generated by room temperature electron tunneling. Another potential test uses a microfluidic chip in a cartridge and isothermal amplification. Results can be read and uploaded to a smart phone.

The actual impact of these new technologies still need to be ascertained, yet, they provide a snapshot of innovative testing, not only for SARS-CoV-2, but  for other pathogens. Rapid point of care tests could ultimately be used for screening a large group of people (i.e., airline passengers, concert attendees) especially if they can be linked to smart phones. This could be an important interventional strategy in preventing transmission of the virus and in preparing for future pandemics.

 

  1. L. Azzi et al., Saliva is a reliable tool to detect SARS-CoV-2. J Infect 81, e45-e50 (2020).
  2. M. Baghizadeh Fini, Oral saliva and COVID-19. Oral Oncol 108, 104821 (2020).
  3. K. K. To et al., Consistent detection of 2019 novel coronavirus in saliva. Clin Infect Dis, (2020).
  4. J. P. Broughton et al., CRISPR-Cas12-based detection of SARS-CoV-2. Nat Biotechnol 38, 870-874 (2020).

 

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A Statement From the Leadership of the Global Virus Network on the Passing of Renowned Chinese Virologist Yi Zeng

A top cancer researcher and leader in public service is mourned

Baltimore, Maryland, USA, July 23, 2020:  The Global Virus Network (GVN), a coalition comprised of the world’s preeminent human and animal virologists from 55 Centers of Excellence and 10 Affiliates in 32 countries, collectively mourns the passing of Professor Yi Zeng, MD, Academician of the Chinese Academy of Sciences, former President of the Chinese Academy of the Preventive  Medicine and former Dean of the College of Life Science and Bioengineering at Beijing University of Technology. Prof. Zeng was best known for establishing the relationship of Epstein-Barr virus (EBV) and nasopharynx cancer, developing EBV serologic tests for nasopharynx cancer early diagnosis, and discovering the first example of co-carcinogenesis in humans, when the combination of EBV  infection and particular carcinogenic products derived from Chinese medicines and foods common to Southern China caused nasopharyngeal carcinoma.  Prof. Zeng was a founding Center Director of China’s Global Virus Network Center of Excellence and hosted GVN’s 7th International Meeting in Beijing, China in 2015.

“Prof. Yi Zeng’s loss is a tremendous one not just for China, but all of his colleagues around the world,” said Robert Gallo, MD, The Homer & Martha Gudelsky Distinguished Professor in Medicine, Co-Founder and Director, Institute of Human Virology (IHV) at the University of Maryland School of Medicine and Co-Founder and Chairman of the International Scientific Leadership Board of the Global Virus Network (GVN). “In 2012, IHV faculty unanimously voted to honor Prof. Zeng for his lifetime of leadership in virology and cancer research.  We are saddened by this immense loss and extend our deepest sympathies to his family and friends.”

“We will deeply miss Prof. Yi Zeng, whose scientific vision and commitment to the GVN have been at the heart of the cooperation with China,” said Christian Bréchot, MD, PhD, President of GVN and Professor at the University of South Florida.

“We are all saddened by the passing of Prof. Yi Zeng, the former president of the Chinese Academy of Preventive Medicine, which is the predecessor of China CDC,” said George F. Gao, DVM, DPHIL (OXON), Director General of the Chinese Center for Disease Control and Prevention (China CDC). “He was a true founder of modern Chinese disease control and prevention and public health infrastructure. He will be remembered as a great scientist, a good friend and a thoughtful mentor.”

Prof. Zeng made great achievements by pioneering, two important virology research areas in China, including, tumor virology and HIV,” said Yiming Shao, MD, the Chief Expert on AIDS, China CDC, who was Prof. Zeng’s first Doctor Degree student.  “Prof. Zeng transformed tumor virology through early diagnosis of cancer, thereby saving countless lives.  He also identified the first HIV/AIDS cases and developed initial diagnostic tools in China while educating his countrymen on AIDS prevention.”

In the early 1970s, Prof. Zeng researched the relationship of the EBV and nasopharynx cancer, established a series of EBV serologic test methods for nasopharynx cancer and increased the diagnosis rate of nasopharynx cancer at the early stage from 20-30% to 80-90%. His serological index could predict the occurrence possibility of nasopharynx cancer 5 to 10 years in advance.  He discovered carcinogens in Chinese herbal medicines and foods in areas with a high incidence of nasopharynx cancer in conjunction with EBV to cause nasopharyngeal carcinoma. Prof. Zeng was also the first to establish cell lines from nasopharynx cancers with high differentiation and low differentiation and was the first in the world to prove that the human fetal nasopharyngeal mucus tissues infected with EBV, under cooperative function of carcinogen TPA and butyric acid, could develop human nasopharynx cancer in rodents. This finding provided the first direct evidence that the EB virus could induce nasopharynx cancer and at the same time provided models for studying multiple factors of nasopharynx cancer pathogenesis and their mechanisms.  Since 1984, Prof. Zeng conducted research on HIV and AIDS and proved the introduction of HIV into China by identifying the first cases of AIDS and HIV infection and isolating the first HIV-1 virus in the country. He isolated the first Chinese HIV-1 virus in 1987 and established the rapid diagnosis method for HIV.  Prof. Zeng, with his late wife Prof. Zelin Li, also discovered Chinese herbal medicines that had a high inhibitory activity of HIV replication.

“For over five decades, Prof. Zeng was a leading virologist in China,” said Lishan Su, PhD, Professor of Immunology and Virology. Lineberger Comprehensive Cancer Center, Department of Microbiology and Immunology, School of Medicine, The University of North Carolina at Chapel Hill.  Prof. Su honored Prof. Zeng with a special lecture when he received the IHV’s 2012 Lifetime Achievement Award in Public Service. “His pioneering work in basic/clinical research on human viruses, including EBV and HIV and on public health policy, has saved millions of human lives. Prof. Zeng also played a critical role in establishing/leading the first institute of modern medical virology to train a generation of outstanding molecular virologists. He has been respected by all, will be missed and remembered in China and around the world.”

GVN is a global authority and resource for the identification and investigation, interpretation and explanation, control and suppression, of viral diseases posing threats to mankind. It enhances the international capacity for reactive, proactive and interactive activities that address mankind-threatening viruses and addresses a global need for coordinated virology training through scholarly exchange programs for recruiting and training young scientists in medical virology. The GVN also serves as a resource to governments and international organizations seeking advice about viral disease threats, prevention or response strategies, and GVN advocates for research and training on virus infections and their many disease manifestations.

About the Global Virus Network (GVN)

The Global Virus Network (GVN) is essential and critical in the preparedness, defense and first research response to emerging, exiting and unidentified viruses that pose a clear and present threat to public health, working in close coordination with established national and international institutions. It is a coalition comprised of eminent human and animal virologists from 55 Centers of Excellence and 10 Affiliates in 32 countries worldwide, working collaboratively to train the next generation, advance knowledge about how to identify and diagnose pandemic viruses, mitigate and control how such viruses spread and make us sick, as well as develop drugs, vaccines and treatments to combat them. No single institution in the world has expertise in all viral areas other than the GVN, which brings together the finest medical virologists to leverage their individual expertise and coalesce global teams of specialists on the scientific challenges, issues and problems posed by pandemic viruses. The GVN is a non-profit 501(c)(3) organization. For more information, please visit www.gvn.org. Follow us on Twitter @GlobalVirusNews

 

Media Contact:
Nora Samaranayake, GVN
410-706-1966
[email protected]

Antibody Dependent Enhancement and SARS-CoV-2

When Developing a SARS-CoV-2 Vaccine, Researchers Need to Consider that Antibodies May Enhance Infection Rather than Provide Protection

There is encouraging news from recent clinical trials of SARS-CoV-2 vaccines, including several candidate vaccines that induce neutralizing antibodies with no apparent adverse effects. Their protective efficacy at preventing infections is not yet known, but will be ultimately determined by phase 3 trials. However, there are other potential concerns over vaccine outcomes, one of which is the possibility of inducing antibodies that make infection outcomes worse. One such phenomenon is called antibody dependent enhancement (ADE).

The poster child for ADE is, of course, dengue virus (DENV). Infection with one of the four common serotypes of DENV results in worse outcomes after later infection by a different serotype. Indeed, some tetravalent dengue vaccines mimic a first infection with DENV and cause worse outcomes upon later infection, even though neutralizing antibodies are elicited. It is speculated that a successful immune response to DENV requires a CD8+ T cell response. The recombinant vaccine contains only DENV envelope glycoproteins in the backbone of yellow fever attenuated 17D strain, which can be poor in inducing CD8+ T cell response. Indeed, live attenuated tetravalent DENV vaccines (National Institutes of Health ), which contain all the virion proteins, have provided enhanced protection.

How does ADE work? The most common mechanism appears to occur when a non-neutralizing or poorly neutralizing antibody binds to a virus particle. The fragment crystallizable region (Fc) of the antibody interacts with Fc receptors (FcR) expressed on certain immune cells (i.e., macrophages, B cells, Follicular dendritic cells, natural killer cells, and neutrophils) and some of the complement proteins. This facilitates viral entry into immune cells, shifting the tropism of the virus. If the virus can replicate in macrophages or other FcR-containing cell, it provides new opportunities for viral replication and spreads into neighboring cells. In addition, infection of macrophages can cause adverse immune activities. This phenomenon is often observed when antibody concentrations decrease as a result of waning immunity. In addition, an antibody may neutralize potently at high concentrations but cause enhancement of infection at sub-neutralizing concentrations.

Another way in which vaccination can result in worse disease is by enhanced respiratory disease (ERD). This was seen in children vaccinated against respiratory syncytial virus and involves non-neutralizing antibodies forming complexes that get deposited in airways, thus causing inflammation. There also appears to be priming of cell-mediated immunity towards a Th2 inflammatory type of response.

What are the reasons for thinking that ADE will or will not be a problem with SARS-CoV-2? One example of a coronavirus infection for which ADE seems to present a problem is feline infectious peritonitis virus (FIPV). Kittens inoculated with a vaccinia recombinant vaccine containing the FIPV spike protein developed high levels of non-neutralizing antibodies, but only very low levels of neutralizing antibodies. They suffered far worse infection outcome at a much higher incidence. This phenomenon was not observed when other viral proteins were used instead of spike protein; yet, it should be pointed out that FIPV is an alphacoronavirus, unlike SARS-CoV-2, a betacoronavrus.

There are some data on ADE with SARS-CoV-2-related betacoronaviruses. One study showed that a candidate vaccine containing SARS-CoV-1 spike protein elicited neutralizing antibodies in vaccinated mice. The antibodies, however, potentiated infection of B cells by an FcR-mediated mechanism.  Despite this, the vaccine provided protection to mice, so even though it elicited detectable ADE, it did not cause worse disease. A similar finding was made in hamsters.

ADE activities could be found in SARS-CoV-1-infected humans. Polyclonal antisera or of monoclonal antibodies that bind viral spike (S) protein can facilitate uptake by human monocytic cells via their Fcγ receptors (FcγRs). In the case of Middle Eastern respiratory syndrome coronavirus (MERS-CoV), Fc-mediated targeting has been observed with neutralizing antibodies that bind directly to the receptor-binding domain of S protein. For both viruses, this phenomenon is dependent on antibody concentration.

Low concentrations facilitated ADE, while high concentrations neutralized the virus. In SARS-CoV-1-infected macaques, antibodies to spike protein were associated with fatal acute lung injury, attributed to alterations in pro-inflammatory immune responses. Yan and colleagues found that a monoclonal neutralizing antibody to MERS blocked entry of a MERS-CoV pseudovirus into a typical target cell but facilitated viral entry into cells expressing FcR, such as macrophages, by a canonical viral entry pathway. The effect was attributed to the antibody loosening the spike protein trimeric structure, making it more accessible to proteolytic processing.

What about SARS-CoV-2? What of a vaccine based upon the spike protein alone? Is there a possibility that ADE may play a pathogenic role in natural infection? The reality is that there are far more questions about these possibilities than there are actual data. Epidemiological studies investigating ADE in individuals with multiple SARS-CoV-2 infections or cross-reactivity to common-cold-causing CoVs will likely take several years. One indication comes from the use of convalescent plasma. Administration into COVID-19 patients appeared to be generally safe. This does not necessarily reflect what will happen after vaccination with spike antibody protein or inactivated vaccines. Inoculation with whole inactivated virus protected macaques against subsequent challenge and showed no signs of ADE. Reducing the risk of vaccine-associated enhanced respiratory disease or ADF of replication involves induction of high-quality functional antibody responses and Th1-biased T-cell responses. If antibodies against SARS-CoV-2 with ADE potential are detected, vaccine development efforts can leverage the full suite of modern technologies around epitope mapping, protein design, adjuvant design and delivery to maximize safety. Currently, there are no data showing direct evidence of ADE for SARS-CoV-2 candidate vaccines. The answers will likely come from phase 3 trials, a number of which are underway, in recruitment, or planned. Results are most eagerly awaited.

 

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Further Insights into SARS-CoV-2 Genetic Variability: D614G

Can a single amino acid mutation in the spike protein affect the infectivity and immunogenicity of SARS-CoV-2?

Recently, a great deal of attention has become focused on a specific SARS-CoV2 mutant in which amino acid residue 614 of the spike protein is changed from aspartic acid to the less bulky and more neutral glycine. This mutant, D614G, reported by Korber et al., has become increasingly predominant after first seemingly proliferating in Europe, then spreading rapidly elsewhere. Korber et al. suggested the mutant is more infectious, based on higher viral RNA titers from patients who were infected with it and its rapid prevalence, but it does not appear to be more pathogenic, based upon the clinical pictures of the patients. Residue 614 is not in the receptor binding domain. They suggested that the mechanism of enhanced infectivity could be due to glycine not forming a hydrogen bond with the neighboring spike protein subunit, allowing the subunits to dissociate more readily and thereby facilitating virion fusion with the cell membrane.  There is a stunning virtual reality visualization of this on YouTube.  Korber et al. also reported evidence for recombination between genomes carrying both this mutation as well as other mutations, indicating recombination and simultaneous infection of cells with more than one genotype. Although suggestive, no proof was presented for an actual increase in infectivity by the mutant.

Since that report, several other studies have addressed the issue of infectivity more directly. One caveat related to many of these reports is that they use lentiviral particles pseudo typed with coronavirus envelope proteins. Viral entry is measured by a co-transduced indicator gene, such as luciferase. Although this is thought to faithfully mimic coronaviral entry, it is an inherently artificial system. The general consensus of all these studies is that the G614 variant enters cells expressing the ACE2 receptor better than the D614 variant even though the variable residue is not in the receptor binding domain, that there is no difference in clinical outcome, that infection with the G614 variant results in higher viral RNA titers in nasal swabs, and that there is not a great deal of difference in antibody neutralization (which is good news for vaccine development).

Let’s consider the individual reports separately. Ozono et al. used the lentiviral pseudovirus method to sample five different naturally occurring mutations in the spike protein, including D614G, to characterize their behavior relative to the reference genotype. Their entry characteristics varied from having a lesser to a greater ability to enter cells expressing ACE2 and the protease TMPRSS2 cells, which greatly facilitates SARS-CoV2 entry. Significantly, the D614G mutant showed the most efficient entry. Interestingly, SARS-CoV1 was much more efficient at entry than was SARS-CoV2. They performed an in silico structural analysis that suggested that the SARS-CoV1 spike trimer has a more open configuration that would result in greater accessibility to the ACE2 receptor by the receptor binding domain. They also tested COVID 19 antisera from patients infected with the D614 variant, and showed no detectable differences in neutralization between the D614 and G614 variants.

Hu et al. also used a lentiviral pseudovirus system to analyze the D614G variants. As with Korber et al., they found the G614 variant to be globally distributed. Like Ozono et al., they found about a 2.5-fold increase in entry efficiency by the G614 variant, perhaps due to more efficient protease cleavage of its spike protein. Unlike Ozono et al., they found that a minority of COVID 18 antisera failed to neutralize the G614 variant to the same extent as the D614 variant. However, it is not clear with which variants the serum donors were infected.

Wagner et al. used a more natural but messier approach. They looked at viral loads, as measured by RT-PCR, and clinical status of patients in Washington state infected with either the G614 or D614 variants. They found that patients infected with the G614 variant had higher nasal viral RNA loads, but did not have a more severe clinical picture. The age of the patients infected with G614 skewed slightly younger (~3 years). They also found that G614 became increasingly more prevalent in Washington state over time.

Lorenzo-Redondo et al. (1) reported on patients in Chicago infected with one of what they called three clades of SARS-CoV2. Clade 1, which was introduced from Washington, contains the G614 phenotype, while clades 2 and 3 have the D614 phenotype. The origin of clade 2 was ascribed to Illinois, while clade 3 was introduced from New York. Clade 1 had higher viral loads than clade 2, in agreement with Wagner et al. Interestingly, when bronchial alveolar lavage samples were tested, there was little difference in viral RNA titers between the two clades, suggesting that the increased titers were specific to upper airway tissue. This could be a factor increased spread.

It should be pointed out that all the above results are in the form of preprints. In addition, the methods used to measure entry directly are somewhat artificial. However, taken together directly from patient data, it seems that G614 may in fact be more capable of spreading, perhaps because of more facile entry into cells, perhaps due to better proteolytic processing because of a more open quarternary structure. Fortunately, this mutation does not seem to worsen the clinical outcome of infection, nor does it seem to abrogate recognition by most neutralizing antibodies.

 

References

 

  1. R. Lorenzo-Redondo et al., A Unique Clade of SARS-CoV-2 Viruses is Associated with Lower Viral Loads in Patient Upper Airways. medRxiv, (2020).
  2. Tang, Leyan & Schulkins, Allison & Chen, Chun-Nan & Deshayes, Kurt & Kenney, John. (2020). The SARS-CoV-2 Spike Protein D614G Mutation Shows Increasing Dominance and May Confer a Structural Advantage to the Furin Cleavage Domain. 10.20944/preprints202005.0407.v1.
  3. Grubaugh, N.D., Hanage, W.P., Rasmussen, A.L., Making sense of mutation: what D614G means for the COVID-19 pandemic remains unclear, Cell (2020), doi: https:// doi.org/10.1016/j.cell.2020.06.040.

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Cleveland Clinic and The University of Southern Denmark Join Global Virus Network to Combat Viral Diseases

GVN’s latest additions further bolster its 55 Centers for Excellence, expanding knowledge of viruses and treatment

Baltimore, Maryland, USA, Tuesday, July 7, 2020: The Global Virus Network (GVN), comprising foremost experts around the world in every class of virus causing disease in humans and some animals, today announced the addition of Cleveland Clinic and the University of Southern Denmark, including the Bandim Health Project in Guinea-Bissau, as its two newest Centers of Excellence. GVN is a global authority and resource for the identification and investigation, interpretation and explanation, control and suppression, of viral diseases posing threats to mankind.

“We welcome the inclusion of Cleveland Clinic and the University of Southern Denmark to our network,” said Christian Bréchot, MD, PhD, President of GVN and Professor at the University of South Florida.  “The addition of the renowned Cleveland Clinic will provide expertise and collaboration opportunities for the greater GVN on matters relating to viral-host interactions, including antiviral drug development, immune modulatory therapies and vaccine development.  The University of Southern Denmark will provide a very important contribution to novel approaches for vaccination, and also, it will further increase our outreach in Africa through the Bandim Health Project in Guinea-Bissau.”

Cleveland Clinic, headquartered in Cleveland, Ohio, USA, is a nonprofit, multispecialty academic medical center that integrates clinical and hospital care with research and education. Cleveland Clinic’s health system includes Lerner Research Institute, an integrated research institute performing investigations in basic, translational, and clinical research; Cleveland Clinic Florida Research and Innovation Center in Port Saint Lucie, Florida, which is dedicated to the discovery and advancement of innovative translational research, focuses on immuno-oncology and infectious diseases; and, the newly added Global Virus Network Center in Innate Immunity Research.  Cleveland Clinic has a 30-year history of groundbreaking advances in interferon and cytokine research. Robert Silverman, PhD, Professor at Cleveland Clinic’s Lerner Research Institute will lead this GVN Center.

“We are looking forward to collaborating with other centers in the GVN to work toward fundamental discoveries in host-virus interactions, through shared expertise in a wide range of viral infections,” said Dr. Silverman.  “Furthermore, novel antiviral strategies developed through the GVN may be implemented at Cleveland Clinic.”

The University of Southern Denmark has campuses in seven cities across Denmark and has been an established university for over 50 years. It has recently, as the first university in Denmark, made the 17 United Nations Sustainable Development Goals (SDGs) the focal point for its work as a university. The Bandim Health Project is affiliated with the Department of Clinical Research, which constitutes the university affiliation for all researchers and teachers at Odense University Hospital, Odense. The University of Southern Denmark was selected because of its long history of research into infections and vaccinations. Its key scientific contributions to the field are observations that intensity of exposure is the main determinant of severe viral infections and that vaccines have non-specific effects, affecting susceptibility toward a broad range of pathogens.  The Bandim Health Project works with population-based health research in Guinea-Bissau, one of the world’s poorest countries in West Africa. Christine Stabell Benn, MD, PhD, DMSc, Professor in Global Health at the Department of Clinical Research, University of Southern Denmark, will lead this GVN Center.

“We are honored to be part of this eminent network,” said Dr. Benn. “Vaccines and their non-specific effects may be a very important tool against emerging viral treats, allowing us to bridge the time until specific vaccines can be developed. Much more work needs to be done to understand the non-specific effects, both from an epidemiological and an immunological perspective. As a member of GVN, we will benefit greatly from interacting with the world’s leading medical virologists.”

The GVN enhances the international capacity for reactive, proactive and interactive activities that address mankind-threatening viruses and addresses a global need for coordinated virology training through scholarly exchange programs for recruiting and training young scientists in medical virology. The GVN also serves as a resource to governments and international organizations seeking advice about viral disease threats, prevention or response strategies, and GVN advocates for research and training on virus infections and their many disease manifestations.

About the Global Virus Network (GVN)

The Global Virus Network (GVN) is essential and critical in the preparedness, defense and first research response to emerging, exiting and unidentified viruses that pose a clear and present threat to public health, working in close coordination with established national and international institutions. It is a coalition comprised of eminent human and animal virologists from 55 Centers of Excellence and 10 Affiliates in 33 countries worldwide, working collaboratively to train the next generation, advance knowledge about how to identify and diagnose pandemic viruses, mitigate and control how such viruses spread and make us sick, as well as develop drugs, vaccines and treatments to combat them. No single institution in the world has expertise in all viral areas other than the GVN, which brings together the finest medical virologists to leverage their individual expertise and coalesce global teams of specialists on the scientific challenges, issues and problems posed by pandemic viruses. The GVN is a nonprofit 501(c)(3) organization. For more information, please visit www.gvn.org. Follow us on Twitter @GlobalVirusNews

Media Contact:
Nora Samaranayake, GVN
410-706-1966
[email protected]