8^th International Conference on
Virology, Influenza and Infectious Diseases

Emerging infectious illnesses are those that have recently entered a population, whose incidence or geographic range is rapidly expanding, or which threatens to do so shortly. The World Health Organization warned that infectious diseases are emerging at an unprecedented rate in a report published in 2007. Since the 1970s, over 40 infectious diseases have been discovered, including COVID-19, which is brought on by the SARS-CoV-2 coronavirus, SARS, MERS, Ebola, chikungunya, swine flu, and Zika. Living in more densely populated areas, traveling over distances that are much greater than in the past, and coming into closer contact with wild animals raise severe concerns about the potential for new infectious diseases to spread swiftly and start global epidemics like influenza and many others. Such illnesses pay little attention to international boundaries. The small number of organisms that are capable of effective human-to-human transmission might generate significant national and international concern as potential epidemics or pandemic triggers. They may have a range of therapeutic, societal, and economic repercussions.

Virologists have discovered a receptor known as CD169 (also known as Siglec1) that is only expressed in macrophages and is responsible for the hyper-inflammatory reaction of macrophages following SARS-CoV-2 infection. These results could explain why SARS-CoV-2 infection of macrophages in COVID-19 patients' lungs causes inflammatory reactions. It has been proposed that the severity of COVID-19 illness is influenced by the dysregulation of macrophages during SARS-CoV-2 infection and the excessive production of pro-inflammatory cytokines by these macrophages. However, it is still unknown what causes macrophages to react in a hyper-inflammatory manner. The SARS-CoV-2 receptor ACE2 is not expressed by these macrophages. Rather, a lectin called CD169 that detects the SARS-CoV-2 spike protein helped SARS-CoV-2 enter macrophages.

The virologists propose that the abnormal inflammation linked to severe COVID-19 illness may be influenced by the ongoing activation of viral sensing systems that identify these viral replication intermediates in macrophages. Future study is required, according to the virologists, to examine the molecular specifics of this distinct virus entrance mechanism, the limited virus replication in macrophages, and how this entry mechanism varies from the traditional ACE2-mediated entry pathway. Importantly, it is necessary to take into account treatments that aim to block this alternative viral entry pathway as they may help to lessen the negative consequences of SARS-CoV-2 infection in macrophages.

Medical microbiology and virology (MMV) is concerned with the diagnosis, treatment, and prevention of infection dissemination in hospitals and the community. Even though both of these specializations are lab-based, they are crucial to clinical infection treatment. Medical virologists perform their job in a range of locations, including labs, clinics, hospital wards, and the general public. They deal with challenges brought on by current and developing viruses like SARS and avian flu around the world, as well as HIV/AIDS and other blood-borne illnesses like hepatitis B and C. Medical virologists now have to deal with a new threat called "bioterrorism," which takes advantage of diseases like smallpox.

The seriousness of parasites as pathogens that affect public health, the environment, and the global economy is being recognized more and more. More than three billion people have one or more parasite infections, which cause varying degrees of sickness and mortality. The study of parasitic protozoa, helminths, and arthropods is known as parasitology, and these three groups have historically been the only ones covered. The anatomy, life cycle, and interactions of medical parasites with their hosts and environs are the focus of human parasitology. It is expected that parasitic infections will continue to be difficult to control, demanding increased scientific understanding to enhance control efforts.

A long-needed structural data on HCV lays the way for logical vaccine development by virology researchers against this very challenging target by placing a multitude of prior observations into a structural perspective. Two million Americans are estimated to be among the 60 million persons worldwide who have chronic HCV infections. A "silent" infection caused by the virus usually persists for decades before liver damage is severe enough to cause symptoms. The virus affects liver cells. It is a major contributor to primary liver cancer, chronic liver disease, and liver transplants. Although the virus's origins are unknown, it is believed to have appeared at least a few hundred years ago and spread internationally, particularly through blood transfusions, in the second half of the 20th century.

Although the virus was mostly eradicated from blood banks following its original detection in 1989, it still spreads primarily through intravenous drug users exchanging needles in industrialized countries and through the use of sterile medical equipment in impoverished nations. The most popular HCV antiviral medications are efficient but considerably too pricey for widespread use. A successful vaccination may someday make HCV no longer a problem for public health. But no such vaccine has ever been created, in large part due to the extraordinarily challenging nature of understanding the HCV envelope protein complex, which is made up of the viral proteins E1 and E2.

• Track 5-1  Proteomics of HCV
• Track 5-2  Types of HCV
• Track 5-3  Virus transmission

This study is one of the first to be conducted on humans, and it shows how to increase the body's resistance to HIV even when current conventional therapy is halted. Therefore, we see the study as a critical first step toward treatment. Even though there is currently no therapy for HIV and no vaccine to prevent it, current standard care is quite successful in halting the illness. The so-called antiretroviral medication available to HIV patients today reduces the quantity of the virus in the blood and partially recovers the immunology system. Nevertheless, whether the patient is 10 or 20 years into the course of therapy, the amount of virus in the blood rises within weeks to the same level as before the normal treatment began if the standard treatment is stopped.

According to a study, individuals with HIV who are newly diagnosed and are given monoclonal antibodies in addition to their standard HIV medication experience a quicker decline in viral load after treatment begins and develop better HIV immunity. Additionally, when these individuals stop taking their standard HIV medication, their immune systems can partially or completely suppress the virus.

According to the first successful clinical study in virology, the experiment's underlying assumption is that the monoclonal antibodies aid the immune system in identifying and eliminating the contaminated cells. Additionally, the antibodies attach to viruses that end up in the lymph nodes in bulky complexes, promoting the development of HIV immunity in certain immune cells among other things. By doing this, the body may be able to stop the virus from spreading and "guard" itself from the damage brought on by HIV infection. If the regular course of therapy is stopped, prior clinical studies with investigational drugs have not revealed any appreciable impact on the patient's immunity to HIV or the immune system's capacity to suppress the virus.

• Track 6-1  Virus in hiding
• Track 6-2  Optimized treatment
• Track 6-3  Antiretroviral medication

The deadly Lassa virus is indigenous to West Africa and is mostly spread by rodents. Lassa fever is brought on by the virus; it affects up to 300,000 people a year and often begins with flu-like symptoms before progressing to more serious sickness, death, and long-lasting effects including deafness. The Lassa virus is particularly harmful to expectant mothers since approximately 90% of infections during pregnancy result in death. Glycoproteins are used by Lassa to enter host cells and start an infection. The glycoprotein structure of Hastie provided virologists with an understanding of their opponents. The scientists uncovered precisely how the three antibodies in Arevirumab-3 neutralize the Lassa virus based on the high-resolution structures and several functional experiments.

The area of the glycoprotein is where three molecules (called protomers) come together to form a "trimer," a kind of twisted trefoil, as Hastie describes it. Lassa would normally use this region of the glycoprotein to bind with receptors on host cells, but the latest structure shows how a single 8.9F jumps in and binds to all three protomers simultaneously to block infection. Meanwhile, the neutralizing antibody called 12.1F binds to just one protomer in the three-sided trimer.  12.1F would be abundant in any therapeutic. Each 12.1F antibody can attach to a protomer and move as a trio to help neutralize the virus. The Lassa virus is the target of copies of antibody 37.2D that attach in a way that binds neighboring protomers together. Since the Lassa virus needs to open up its trimer to infect host cells, this antibody activity is a major challenge for the virus. Its entrance mechanism is locked up and impossible to operate with 37.2D on the scene.

• Track 7-1  Glycoproteins and Lassa
• Track 7-2  Transmission and Remedy
• Track 7-3  Antibodies
• Track 7-4  Therapeutical methods

Viral infections is less common in people with Down syndrome, but when they do occur, the sickness they cause is more severe. Increasing levels of an antiviral cytokine type I interferon (IFN-I), which is largely coded for by chromosome 21, are the source of this, according to recent research. Increased IFN-I levels trigger an initial overreaction of the immune system, but the body overcompensates to lower inflammation, leaving the body more vulnerable to viral infection later. While immunological dysfunction is evident in patients with Down syndrome, the exact mechanism by which a supernumerary chromosome 21 results in the dysregulation of defenses is yet unknown.

The virologists studied fibroblasts and white blood cells produced by people with and without Down syndrome at both the mRNA and protein levels to fill this information gap. They concentrated on the chromosome 21-based IFN-I receptor subunits IFNAR1 and IFNAR2, which are powerful antiviral cytokines. Independent of trisomy 21, the virologists discovered that elevated IFNAR2 expression was sufficient to cause the IFN-I hypersensitivity seen in Down syndrome. But afterward, the excessively powerful IFN-I signaling cascade activated a protein called USP18, a strong IFNAR negative regulator, to provide excessive negative feedback. Further IFN-I responses and antiviral responses were subsequently inhibited by this approach. Together, the data show that Down syndrome is predisposed to oscillations of hyper- and hypo-responses to IFN-I, which reduce the incidence of illness and raise infection-related morbidity and death.

• Track 8-1  IFN-I
• Track 8-2  USP18
• Track 8-3  Immune Dysregulation

The development of metatranscriptomics aids in the discovery of key characteristics of the Earth's RNA virome. Virologists found many new viruses in this study that shed light on the variety, host range, and evolution of RNA viruses. The discovery of 2.5 million RNA virus-derived sequences came through the mining of more than 5,150 different metatranscriptomes from existing sources. The variety of known RNA viruses has increased five times as a result of this development. The most unique populations are divided into two groupings that might constitute new phyla, while others are categorized into multiple new classes and orders. The most significant finding is the sharp rise in the variety and quantity of bacteria-infecting viruses, which are now known to make up a far larger proportion of RNA viruses than previously believed. A significant resource for RNA virology should be the enormous collection of novel RNA virus genomes, which offers insight into the evolution of RNA viruses.

• Track 9-1  Metatranscriptomics
• Track 9-2  RNA virome
• Track 9-3  Metagenomics and Metatranscriptomics
• Track 9-4  SAMSA2

Despite having well-controlled HIV illness, a new study in the field of virology from Zambia shows that children with HIV are considerably more likely to do poorly on neurological tests, raising the possibility that they may have cognitive and mental health problems. However, early intervention is also suggested by the studies. Children who are exposed to the virus before birthing are known to have an increased risk of developing neurocognitive and mental issues, such as depression, when they get older. HIV continues to be a significant worldwide health burden. HIV has a disproportionately large impact on Sub-Saharan Africa, accounting for over 70% of all infections worldwide. Even though combination antiretroviral treatment (cART) is widely available, many infected children continue to experience the neurocognitive and mental abnormalities that are linked to HIV, including depression and delayed academic development. Findings imply that one of the most crucial things we can do is identify children with HIV early and start them on antiretroviral medication since children perform considerably better intellectually if they don't get ill from HIV. The dietary component is another important element in this.

• Track 10-1  Neurology and virology
• Track 10-2  Vacuolar myelopathy
• Track 10-3  Lymphomas

The terrible enterovirus family, which includes numerous common colds, includes the poliovirus. Since technology has not yet enabled us to see thus deeply within the cells, it has been known for some time that enteroviruses significantly reorganize the inside of infected hosts. Virologists have now been able to capture three-dimensional pictures of how the poliovirus develops and colonizes human cells for the first time thanks to a recent study. By observing areas with half-assembled viruses, the virologists were able to pinpoint the location in the cell where the poliovirus creates new virus particles. This " factory" in the cell, which resembled autophagy, a normally occurring cellular process, turned out to be present. The 2016 Nobel Prize in Physiology or Medicine was awarded for the discovery of the cell mechanism called autophagy.

Autophagy often works to destroy substances that the cell wishes to get rid of, such as virus particles. However, the poliovirus can rewire this anti-virus defensive system such that it instead creates additional viruses. The scientists discovered that some proteins are particularly significant. The virus uses the VSP34 protein to create new particles. When the virologists blocked VSP34, they could observe that the virus could mainly only form half particles and could seldom assemble whole viruses. ULK1, another significant protein, inhibits the development of viruses. The number of viruses multiplied, as the virologists could observe when this protein was suppressed. Given that the illness was seen as nearly eliminated, a fall in vaccination rates as well as rising vaccine resistance may be contributing factors in wealthy nations where polio has returned.

• Track 11-1  Poliomyelitis
• Track 11-2  Post-polio syndrome
• Track 11-3  Types
• Track 11-4  Brain Physiology

Despite the immune system's extensive defensive network's outstanding strength, one kind of threat is particularly difficult to eliminate. This develops when the body's cells go renegade, which causes the cancer phenomena. A recent study describes how employing the myxoma virus in combination with immunotherapy and virotherapy offers patients with cancer that are resistant to treatment fresh hope. The strategy combines two strategies that have each had significant success in treating certain malignancies. The study in virology explains how oncolytic virotherapy, a method that employs viruses to combat cancer, can work in conjunction with currently used immunotherapy methods to enhance the immune system's ability to effectively target and eradicate cancer cells. The immune system is made up of a variety of specialized cells that are created to patrol the body and react to dangers.

The immune system is engaged in an ongoing arms race with infections as they develop complex strategies to evade immune protection, spread throughout the body, and lead to disease. The new study emphasizes how immunotherapy can overcome the cancer resistance barrier when it is combined with virotherapy, specifically using T cells that have been infected with myxoma. Myxoma can directly target and destroy cancer cells, but it is more beneficial when it causes autolysis, a peculiar type of T-cell-directed cell death.

 Apoptosis and pyroptosis, two other types of programmed cancer cell death generated by T-cells, are strengthened by this type of cell death. Cancerous cells nearby the ones the therapy is targeting are also eliminated during myxoma-mediated autosis, a process known as bystander death. Even in solid tumors that are notoriously difficult to cure, this action can significantly increase the aggressive eradication of cancer cells by dual therapy. To allow CAR T-cells or TCR cells to infiltrate the tumor environment, grow, and activate, a combined myxoma-immunotherapy method has the potential to convert so-called "cold tumors," which avoid immune system identification, into "hot tumors," which immune cells can recognize and eradicate.

• Track 12-1  Viral immunotherapy
• Track 12-2  Oncolytic Viruses.
• Track 12-3  Friendly Viruses
• Track 12-4  Cancer cells
• Track 12-5  Myxoma

The body's first line of defense against any foreign invader is triggered when a particular enzyme, present in all cells, is blocked, according to studies conducted on mice and cell cultures. This reaction significantly reduced particle proliferation when tested by several virus types in the study and shielded mouse lungs from injury. This discovery was made possible in part by a method the virologists developed to pinpoint the site of an RNA alteration they were researching and to identify the enzyme responsible for the change. They were able to deduce from the mapping that this enzyme functions in mammal hosts, not viruses, who wish to infect them. Human respiratory syncytial virus and human metapneumovirus, two viruses that can cause serious respiratory infections in young children and the elderly, as well as the Sendai virus from mice, the vesicular stomatitis virus found in cattle, and the DNA virus herpes simplex were all tested against the immune response in this study. The virologists reported early findings from prior investigations in cell cultures revealed the SARS-CoV-2 virus may be similarly controlled by this antiviral approach. Replication and gene expression of all of these viruses were dramatically decreased when the enzyme was stopped. To start the immune system's reaction, the RNA alteration known as cytosine-5 methylation, or m5C, has to be changed. It is one of around 170 documented chemical alterations to RNA molecules seen in living things that have an array of effects on biological processes.

• Track 13-1  Broad-spectrum antivirals
• Track 13-2  Cytosine-5 methylation
• Track 13-3  Respiratory syncytial virus
• Track 13-4  Human metapneumovirus

This research in virology is a phase III clinical trial that is randomized, double-blinded, multi-center, and placebo-controlled for individuals ages 18 to 59. This investigation's goal is to assess the SARS-CoV-2 inactivated vaccine's effectiveness, safety, and immunogenicity. Sinovac Research & Development Co., Ltd. produced both the experimental vaccination and a placebo. 13.000 subjects in total will be registered. On the scheduled day of day 0,14, the subject will either be given two doses of the experimental vaccination or a placebo. The trial will involve two distinct cohorts, as anticipated.

 Healthcare professionals in the high-risk category (K-1) will make up the first cohort, while those at normal risk will make up the second cohort (K-2). After 1300 participants have had their second round of vaccination, the safety data will be reviewed by the data safety monitoring board without compromising the blinding process. If there are no safety concerns, the K2 cohort will continue to receive vaccinations. The K-1 cohort will have 1.300 participants, 650 of whom will participate in the SARS-CoV-2 vaccination and placebo arms. It was intended to include 7.650 participants in the SARS-CoV-2 vaccination group and 3.500 volunteers in the placebo group in the K-2 cohort (the typical risk category for COVID-19).

• Track 14-1  Discovery
• Track 14-2  Phases
• Track 14-3  Immunogenicity
• Track 14-4  Stages

The EBV virus goes latent in the body after infection, although it can occasionally be reawakened. It is the main cause of infectious mononucleosis and is linked to multiple sclerosis, Hodgkin lymphoma, and several malignancies, including Hodgkin lymphoma. Severe symptoms and problems from EBV infection are more common in immunocompromised individuals than in immunocompetent individuals, such as transplant patients. The scientists create several experimental mAbs that target two important proteins called gH and gL that are present on the surface of EBV. The two proteins are known to facilitate EBV infection and fusion with human cells. When the investigational mAbs were tested in a lab setting, human B cells and epithelial cells, which line the throat at the initial site of EBV infection, were not infected by EBV. Virologists found several vulnerable locations to target by analyzing the structure of the mAbs and their two surface proteins using X-ray crystallography and advanced microscopy. One of the experimental monoclonal antibodies, known as mAb 769B10, offered nearly full protection against EBV infection in mice. Additionally, the mAb prevented EBV lymphoma in all examined animals. The results demonstrate promising EBV vaccine targets and the potential of investigational mAbs to prevent or treat EBV infection in immunocompromised patients most vulnerable to severe EBV-related illness.

• Track 15-1  Myeloma cells
• Track 15-2  EBV
• Track 15-3  IgG
• Track 15-4  Monoclonal

In the globe, IAVs cause between 250,000 and 500,000 fatalities annually. An immune response made up of several molecular mechanisms starts when IAV infects its host. IAV may infect a variety of species, and although certain host responses are common, physiological and genetic variations among these species can influence these responses. The study identified several important defensive mechanisms particular to tissues and species by using RNA sequencing to assess gene expression over time in cells and tissues taken from IAV-infected humans, ferrets, and mice. It has been demonstrated that the Tudor domain-containing protein, a kind of protein implicated in epigenetic regulation, encoded by the gene TDRD7 plays a crucial role in the immunological defense mechanisms against IAV in all species. After making this finding, the virologists carried out additional studies in which they inhibited the activity of TDRD7, which led to an increase in viral replication in IAV-infected mice. To create flu treatments that work, it is crucial to understand both common and species-specific reactions to influenza. This information may also be used to guide future studies on other respiratory illnesses like COVID-19.

• Track 16-1  TDRD7
• Track 16-2  Tudor domain-containing protein
• Track 16-3  Antigenic drift
• Track 16-4  Pathophysiology
• Track 16-5  Antiviral chemoprophylaxis
• Track 16-6  Prognosis
• Track 16-7  Epidemiology
• Track 16-8  Etymology

The current North American epidemic has affected over 40 species of birds, including raptors like owls and hawks as well as songbirds like crows and sparrows. Compared to the North American epidemic in 2014, this one is affecting a wider variety of species and has a larger geographic reach. Despite being zoonotic, there is extremely little risk to humans from avian influenza. People who often handle birds, such as wildlife professionals, poultry workers, or home chicken owners, are at a slightly higher risk. The first human case of avian influenza in North America during this outbreak was recently identified in a guy in Colorado. He was involved in the culling of chickens and contracted an infection from a sick fowl. He experienced little symptoms, was kept isolated, and made a full recovery, according to the Centers for Disease Control and Prevention. His minor symptoms are a matter of concern since, as Hill points out, it makes the virus more difficult to detect and monitor because infected people may disregard their weak symptoms and forego medical attention, much with COVID-19.

The 2014 bird flu pandemic eventually subsided, but the 2022 outbreak is very different from the previous outbreak, according to him, therefore that won't likely happen this time. In contrast to this epidemic, the viruses discovered in North America in 2014 only comprised fragments of the highly dangerous H5 viruses. Also, it appears that this assault has expanded more quickly than the previous one. In addition, according to Hill's study, avian flu epidemics tend to grow in size and frequency over time.

• Track 17-1  Paramyxoviruses
• Track 17-2  Metapneumoviruses
• Track 17-3  Reovirus
• Track 17-4  Leukosis Virus
• Track 17-5  Avian viruses

For thousands of years, viruses and viral infections have been the focus of research, agriculture, and medicine. Some of our greatest struggles and achievements have involved virology. Many methods used to examine cellular genes, such as restriction enzyme mapping, molecular cloning, and genome sequencing, were initially created and refined by utilizing smaller and more manipulable viral genomes. Indeed, virology laboratories served as the breeding ground for the fields of genetic engineering and biotechnology.

 Viruses and viral gene products have also become important tools for understanding many biological processes and, possibly, for the treatment of illness. These techniques include reverse transcriptase, which is used to create cDNA, viral vectors, which transmit genes and produce proteins, transgenic animals, vaccines, and oncolytic treatment, which aims to leverage some viruses' ability to selectively target and destroy cancer cells. Studies are being conducted to see if this method is effective in treating human tumors. In a recent study, all mice given the protein-based immunization survived when exposed to lethal doses of the COVID-19-causing SARS-CoV-2 virus.

 The SARS-CoV-2 exposure did not result in any lung damage in any of the mice. During a 14-day trial, every mouse who did not receive the nanoparticle vaccine perished. The nanoparticles that contain the immunological target are known as SNAs, and they are a kind of globular DNA that can infiltrate immune cells and excite them very well. Over 60 different cell types have been used to evaluate SNAs. The ideal ratio between the density of the SNA's shell and core that yields the strongest response was established experimentally. SNA vaccines have been used to treat triple-negative breast cancer in mice, and more cancer-related vaccines are currently being developed. It was mostly practical to use COVID-19 as a case study to contrast how well the vaccine performed. However, it also draws attention to the SNA's larger significance as a platform for infectious diseases.

 Although the case study's results are quite impressive, the intention was not to outperform the COVID vaccines currently on the market. Since there will eventually be another emergent disease, we are preparing for the next mutation or the next illness that requires a highly structured vaccine.

• Track 18-1  Innovation
• Track 18-2  Future pathway
• Track 18-3  Upcoming Techniques
• Track 18-4  Mutating virus

Emerging irresistible infections are defined as infections that have recently appeared in a population, are becoming more frequent or widespread geographically, or are taking measures to do so. The World Health Organization cautioned in a report from 2007 that infectious diseases are spreading at an unusually rapid rate. Since the 1970s, over 40 infectious diseases have been discovered, including COVID-19, which is caused by the SARS-CoV-2 Covid, SARS, MERS, Ebola, Chikungunya, and avian, pig, and Zika influenza. Traveling more frequently and over longer distances than before, living in more densely populated areas, and coming into closer contact with wild animals all increase the risk of new infectious diseases spreading quickly and causing widespread pandemics, which is a serious issue. Such diseases don't pay much attention to waiting in queues. As potential plague or pandemic causes, the small number of organisms capable of effective human-to-human transmission might raise substantial public and global concerns. They may provide a range of financial, cultural, and healing effects.

• Track 19-1  Monitoring and Seroprevalence
• Track 19-2  Infectious disease recurrence
• Track 19-3  Disease transmission and global health
• Track 19-4  Clinical Characteristics and Results