Navigating the Upcoming Cold/Flu Season in the Midst of the SARS-CoV-2 (Coronavirus) Pandemic

administrating flu shotName: Zheng Xing

Job Title: Associate Professor

Background: 

I obtained my Ph.D. in Microbiology and Immunology at Cornell University and my research interest has been in the field of emerging viral pathogens and viral pathogenesis. I have worked on a number of viruses including avian influenza virus, a novel bunyavirus, and Zika virus and tried to understand the mechanism how these viruses interact with the host cells and the host responds to the virus leading to pathological consequences.

What are your current research projects?

In the past years I have focused on studying the novel bunyavirus that causes a mysterious disease, severe fever with thrombocytopenia syndrome (SFTS), emerging since 2007 among farmers with a fatality rate up to 15% in China. We showed that the virulence of SFTS bunyavirus was related to its suppression of host immunity and the nonstructural protein, NSs, was the key to the viral suppression of the host innate response. We demonstrated the mechanism by which NSs interacts with TBK, a key kinase in the induction of the interferon signaling pathway by sequestering TBK into a viral inclusion body, a unique structure made by NSs, in infected cells, resulting in the blockage of interferon induction. The finding was considered to be “significant in unveiling a novel mechanism for viral immune evasion” in a “Spotlight Feature” by the Journal of Virology.

We have further characterized the inclusion bodies formed by viral NSs to be essentially lipid droplets, which, however, was reconstructed by NSs in the cells infected by the bunyavirus. A host protein, synaptogyrin-2, was identified to play a critical role in the reconstruction of the lipid droplets during infection. Recently we showed that NSs interacts directly with IRF7, another transcription activation, and sequesters it into the inclusion bodies, blocking an induction of IFN-a as well as IFN-b, while IFN-a appears to be unique in antiviral immunity in hemopoietic cells against SFTS bunyavirus.

 What is your stance on the upcoming cold/flu season, especially while during the COVID-19 pandemic?

The COVID-19 pandemic has changed a lot of things, including the seasonal epidemic of common cold and influenza. We have seen a significant lower prevalence of influenza virus in the beginning weeks of the 2020-21 flu season in comparison to the regular ones. According to the CDC Weekly Report on December 13, 2020, the percentage of visits for influenza-like illness (ILI) remained at 1.6% for the fourth consecutive week, below the baseline of 2.6%. While normally the rates have already started to increase rapidly in this time, the incidence of ILI has shown no tread to go up for now in the US and almost all fifty states are in the minimal ILI activity level. Although it is still impossible to predict whether the seasonal influenza would be less prevalent in the Northern Hemisphere this season, we learnt that the seasonal flu was barely detected in Australia and other countries in the Southern Hemisphere when these countries were hit hard by COVID-19 during the past summer (their winter season). In contrast to the seasonal flu, the common cold may not be impacted much by COVID-19.

How COVID-19 affects the prevalence of the common cold or flu remains to a question. We have known little about how SARS-CoV-2 interacts with the common cold and influenza viruses. We knew that SARS-CoV-2 is more contagious than influenza virus. The city lockdown and policies for social distancing and facial mask wearing would prevent influenza virus from transmission in humans to certain degree. International travel ban probably plays an important role in halting influenza transmission. The flu virus could have been effectively blocked from the countries from the Northern to the Southern Hemispheres in the late spring or early summer when the borders were closed globally.  The virus, already in a much lower level up to 95% decrease from the normal, would be further blocked from the Southern back to the Northern Hemispheres in the autumn or early winter. It remains to be a mystery that Influenza virus is seasonal but SARS-CoV-2 is not.

The common cold could be caused by many respiratory viruses including rhinoviruses, adenovirus, and coronaviruses. During the COVID-19 pandemic, somehow rhinoviruses dominate in causing common cold, which occurred early in Australia and now in the US. There are over a hundred serotypes of rhinoviruses and their toughness to the environment is considered to be a factor for its prevalence because rhinoviruses do not have an envelope unlike coronaviruses. Prevalence of rhinoviruses increased greatly since September when schools opened. Probably kids are the key for transmitting rhinoviruses in communities and families.

Recent studies have indicated that people suffering from the common cold may benefit from being less infected by, or having a milder illness after infection of, SARS-CoV-2. There might be some explanations for this. First, infection with the common cold coronavirus could produce immunity cross-reactive against COVID-19. Antibodies induced from some common cold coronavirus could show neutralizing activities against SARS-CoV-2, while cell-mediated immunity triggered from the identical epitopes shared in viral proteins of both viruses could also be beneficial to patients’ recovery. Second, infection of rhinoviruses is considered to induce host resistance to SARS-CoV-2 through a mechanism called viral interference. This is the phenomena found in many other virus infections, both in human and animals. A current antiviral therapeutic project led by Pomeroy Endowed Chair and VBS Professor, Carol Cardona is about using infection of Newcastle disease virus (NDV) for prevention of high pathogenic avian influenza virus in turkeys through viral interference.

Flu prevalence may change and increase, however. In a normal year the full swing of a flu epidemic occurs usually a few weeks or months later.  Thus it is not the time to say flu is not going to be a problem during this COVID-19 pandemic.

What should people expect and how can they be better prepared for the cold/flu season?

We could not underestimate the seasonal flu in the upcoming weeks and months during COVID-19 pandemic. People could be infected with flu virus and those in the vulnerable groups or with pre-existing conditions would have serious complications if infected. Co-infection of SARS-CoV-2 and influenza virus has been found in patients in the US. Hospitals have been overloaded and ICUs are nearly full across the country because of COVID-19. Serious ILI would further burden medical workers and hospitals and deteriorate the health system.

Flu vaccination is highly recommended to people, especially those in the vulnerable categories or with existing conditions this season. About half the population over 6 months are immunized with flu vaccine each year in the US, which provides protection against infection, reduces the risk of illness, hospitalization and even the risk of deaths. There are trivalent and quadrivalent flu shots, with each viral seed strain updated or changed based on the 2019 isolates in the field. An additional influenza B virus is added to the quadrivalent formula this year.

Goals for 2021:

We are continuing our work on SFTS bunyavirus in two fronts. First, SFTS bunyavirus appears to cause viral encephalitis but the target cell types in the brain and viral pathogenesis are unclear. We are collaborating with researchers in China CDC to understand the roles of astrocytes and microglial cells in viral pathogenesis. Second, multiple organ failure occurs in almost all fatal patients with SFTS. We have furthered our studies on activation of inflammasome and pyroptosis in immune cells and will try to analyze how platelets are impacted by the viral infection. We postulate that platelets could be activated through unknown mechanisms that would lead to cytokine storm and systemic thrombosis, which depletes platelets and results in dissimilated intravascular coagulation, deteriorated by pyroptosis in infected monocytes.

I have a passion for teaching and hope to continuously contribute to undergraduate and graduate education. I participated in team-taught courses including microbiology and mechanism of animal diseases. I taught an undergraduate Honors Seminar entitled “Microbes and Civilization”, which was built on knowledge about microbes and epidemics and my profound interest in human history and civilization. If the Undergraduate Honors Program approves of my updated course proposal, which requires approval yearly, I will be very happy to offer it next year.