Pandemic Influenza. While the molecular and epidemiological effects of influenza infection in pulmonary tissue are well-documented, the effects of infection in other organs remains unclear. Several clinical and experimental studies have shown influenza virus to be cardiotropic, with virus disseminating from the lungs to cardiac tissue early after severe infection. The scientific premise for these studies comes from the extensive clinical evidence of aberrant cardiac pathologies (myocarditis, ischemia, cardiac dysfunction, and other major adverse cardiac events) associated with influenza infections, with these being more pronounce during pandemics. Our overall hypothesis is that acute viral infection leads to localized inflammatory and metabolic changes that promote the development of major adverse cardiac events that persist through convalescence. In our studies we propose to link the effector proteins of influenza viruses to the aberrant cardiac changes observed during in vivo infection, the role of cell death pathways in it, and characterize the long-lasting effects of such and the role pre-existing cardiac disease in such with the purpose of developing new therapies to prevent respiratory virus-induced cardiac complications. Most importantly, in the development of novel therapeutic or vaccine candidates it is essential to understand the full spectrum of the pathogenesis of an organism such as influenza viruses, an area currently understudied.
SARS-CoV-2 infection. The global pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has had great effects in the overall health of infected and convalescent patients. While immediate medical attention had been dedicated to respiratory illness and lung infection, more and more clinical evidence is revealing a wide range of systemic manifestations by the virus, of which one includes cardiac injury (e.g., heart attack or arrhythmia). Recent reports have indicated a potential direct role for SARS-CoV-2 in causing myocarditis, fatal arrhythmias and other major adverse cardiac events as viral particles are present in the cardiac tissue of patients that succumbed to infection. Moreover, recently discovered variants have shown greater infectivity and exacerbation to cardiac complications. We aim to define the cellular and molecular mechanisms that modulate SARS-CoV-2 cardiac pathogenesis.