Avian influenza virus circulation and immunity in a wild urban duck population prior to and during a highly pathogenic H5N1 outbreak.

Highly pathogenic avian influenza (HPAI) H5N1 clade 2.3.4.

Longitudinal screening of retail milk from Canadian provinces reveals no detections of influenza A virus RNA (April-July 2024): leveraging a newly established pan-Canadian network for responding to emerging viruses.

Highly pathogenic avian influenza (HPAI) H5N1 has caused the deaths of more than 100 million birds since 2021, and human cases since 1997 have been associated with significant morbidity and mortality. Given recent detections of HPAI H5N1 in dairy cattle and H5N1 RNA detections in pasteurized retail milk in the United States, we established the pan-Canadian Milk Network in April 2024. Through our network of collaborators from across Canada, retail milk was procured longitudinally, approximately every 2 weeks, and sent to a central laboratory to test for the presence of influenza A virus RNA.

Sequence Matters: Primary COVID-19 Vaccination after Infection Elicits Similar Anti-spike Antibody Levels, but Stronger Antibody Dependent Cell-mediated Cytotoxicity than Breakthrough Infection.

Infection before primary vaccination (herein termed "hybrid immunity") engenders robust humoral immunity and broad Ab-dependent cell-mediated cytotoxicity (ADCC) across SARS-CoV-2 variants. We measured and compared plasma IgG and IgA against Wuhan-Hu-1 and Omicron (B.1.

Inflammatory Consequences: Hepatitis C Virus-Induced Inflammasome Activation and Pyroptosis.

Hepatitis C virus (HCV), despite the availability of effective direct-acting antivirals (DAAs) that clear the virus from >95% of individuals treated, continues to cause significant health care burden due to disease progression that can lead to fibrosis, cirrhosis, and/or hepatocellular carcinoma. The fact that some people who are treated with DAAs still go on to develop worsening liver disease warrants further study into the immunopathogenesis of HCV. Many viral infections, including HCV, have been associated with activation of the inflammasome/pyroptosis pathway.

Characteristics of Vaccine- and Infection-Induced Systemic IgA Anti-SARS-CoV-2 Spike Responses.

Mucosal IgA is widely accepted as providing protection against respiratory infections, but stimulation of mucosal immunity, collection of mucosal samples and measurement of mucosal IgA can be problematic. The relationship between mucosal and circulating IgA responses is unclear, however, whole blood is readily collected and circulating antigen-specific IgA easily measured. We measured circulating IgA against SARS-CoV-2 spike (S) to investigate vaccine- and infection-induced production and correlation with protection.

Cellular Immune Responses to SARS-CoV-2 in Exposed Seronegative Individuals.

Some SARS-CoV-2-exposed individuals develop immunity without overt infection. We identified 11 individuals who were negative by nucleic acid testing during prolonged close contact and with no serological diagnosis of infection. As this could reflect natural immunity, cross-reactive immunity from previous coronavirus exposure, abortive infection due to de novo immune responses, or other factors, our objective was to characterize immunity against SARS-CoV-2 in these individuals.

The 11th Canadian Symposium on Hepatitis C Virus: 'Getting back on track towards hepatitis C elimination'.

Hepatitis C virus (HCV) affects approximately 204,000 Canadians. Safe and effective direct-acting antiviral therapies have contributed to decreased rates of chronic HCV infection and increased treatment uptake in Canada, but major challenges for HCV elimination remain. The 11th Canadian Symposium on Hepatitis C Virus took place in Ottawa, Ontario on May 13, 2022 as a hybrid conference themed 'Getting back on track towards hepatitis C elimination.

Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis.

It is well-known that viruses activate various inflammasomes, which can initiate the programmed cell death pathway known as pyroptosis, subsequently leading to cell lysis and release of inflammatory cytokines IL-1β and IL-18. This pathway can be triggered by various sensors, including, but not limited to, NLRP3, AIM2, IFI16, RIG-I, and NLRC4. Many viruses are known either to activate or inhibit inflammasomes as a part of the innate immune response or as a mechanism of pathogenesis.

Moderate to severe SARS-CoV-2 infection primes vaccine-induced immunity more effectively than asymptomatic or mild infection.

Hybrid immunity induced by vaccination following recovery from SARS-CoV-2 infection is more robust than immunity induced by either infection or vaccination alone. To investigate how infection severity influenced the strength and character of subsequent vaccine-induced humoral or cellular immune responses against SARS-CoV-2, we assessed humoral and cellular immune responses against SARS-CoV-2 following recovery from infection, vaccine dose 1 and vaccine dose 2 in 35 persons recovered from COVID-19. Persons with polymerase chain reaction or serologically confirmed SARS-CoV-2 infection were recruited into a study of immunity against SARS-CoV-2.

Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death.

Extensive inflammation in the liver is known to contribute to the pathogenesis of hepatitis C virus (HCV) infection. Apoptosis has, for a long time, been known to act as a mechanism of hepatocyte death, but our previous research also identified inflammasome-mediated pyroptosis in infected and uninfected bystander cells as an additional mechanism of HCV-induced cytopathicity. The purpose of this study was to investigate the mechanism of HCV-induced cell death and to determine the timing and relative contributions of apoptosis and pyroptosis during HCV infection.