Kefeng Qin, MD, PhD, is professor and Chief Scientist in Huzhou Central Hospital, the affiliated Huzhou hospital Zhejiang University School of Medicine. He has been working at NIH, the University of Toronto, Northwestern University, the University of Maryland, and the University of Chicago as a scientist in the field of virology, including HSV, HIV, and SARS-CoV-2 research, and neurodegenerative diseases, including prion, doppel, and Alzheimer’s disease. Research papers have been published in Nature, JBC, JNS, etc.
Following the COVID-19 pandemic caused by SARS-CoV-2, the phenomenon of immune debt has emerged worldwide, significantly changing the epidemiology of respiratory infections. Acute respiratory viral infections (ARVIs) are the leading cause of morbidity and mortality in children worldwide and have a significant impact on the health of adult patients. The post-COVID-19 model of ARVI remains largely unstudied internationally. In order to study the epidemiology of ARVI in the second year after the COVID-19 pandemic, we examined the ethology of patients with fever in our hospital from June to August 2024. Among the total 12,108 febrile patients, 5,734 (47.4%) were males, 6,373 (52.6%) females, 4,803 (39.7%) children (aged ≤ 12 years), and 7,303 (60.3%) adults (aged ≥ 13 years). The total number of patients who were positive for 7 pathogens was 7,167 (59.2%), including 2,094 cases (17.3%) of adenovirus (ADV), 1,295 (10.7%) of human rhinovirus (HRV), 984 (8.1%) of Mycoplasma pneumoniae (MP), 2,433 (20.1%) of SARS-COV-2, and 349 (2.9%) of influenza A virus (IAV). There were 3 cases of influenza B virus (IBV) and 9 cases of respiratory syncytial virus (RSV). There is also co-infection with some pathogens. ADV and SARS-CoV-2 infections account for a large proportion. There is also co-infection with some pathogens. We have further analysed the distribution of cases in ARVI patients in the 13 weeks from June 1 to August 31, 2024, and found that during the week of July 21-27, there was a spike in febrile patients, which was mainly due to the outbreak of SARS-CoV-2 infection. Other pathogens, including ADV, HRV, MP, and IAV, were circulating at low levels and did not record a new peak of infection. Multiplex immunoassays were performed on the plasma of patients with positive nucleic acid or co-infection of 7 pathogens, nucleic acid-negative patients with fever, and health volunteers. The concentration level data of 48 factors of immunity and inflammation were obtained. The data were analysed using ANOVA and post-hoc Tuley HSD tests, and it was found that pathogen infection led to changes in the levels of some factors. The immune or inflammation reactions were divided into three groups. Levels of CTACK, G-CSF, IFN-a2, IL-1ra, IL-4, IL-6, IL-12p40, MIF, MIP-1b, SCGF-b, TRAIL, or VEGF presented with very significant differences in different pathogen infections (P<0.01). Levels of GRO-a, HGF, IL-1a, IL-2Ra, IL-9, IP-10, MIG, or TNF-b were increased in patients with fever, but there were no significant differences between different pathogen infections (P<0.01). Levels of eotaxin, FGF, GM-CSF, IFN-g, IL-1b, IL-2, IL-3, IL-5, IL-7, IL-8, IL-10, IL-12(p70), IL-13, IL-15, IL-16, IL-17, IL-18, LIF, MCP-1, MCP-3, b-NGF, PDGF-bb, RANTES, or SCF did not change with significant differences with different pathogen infections (P > 0.05). Based on these results, we have found that the epidemiological and immune response profile of ARVI is unique and complicated. Our finding would help the clinical manifestations and management strategies.