Objective:To understand the epidemiological and clinical characteristics of human infection with avian influenza A(H3N8) virus and the molecular biological characteristics of the pathogen, and provide scientific evidence for the prevention and control of human infection with avian influenza A(H3N8) virus.Methods:An epidemiological investigation was conducted for a case of human infection with avian influenza A(H3N8) virus in Changsha in May 2022 to collect the information about exposure history, route of infection, onset and treatment, potential contacts and other possible exposures for a descriptive analysis. Nucleic acid detection and gene sequencing were used to detect the pathogen and analyze the genetic characteristics.Results:The case had a history of exposure to live poultry trading market 6 days before the onset of illness. Subtypes H3 and N8 of avian influenza virus were detected in live poultry markets. Deep gene sequencing showed that the virus had adaptive mutations in mammals, reduced sensitivity to alkamine agent, and no resistance mutations related to neuraminidase inhibitors and polymerase inhibitors were detected.Conclusion:The case was infected due to exposure to the live poultry market environment contaminated by avian influenza A(H3N8) virus, and no human to human transmission was found.

Pancreatic cancer induced by mutation KRAS exhibited a higher risk of incidence, recurrence and mortality. C-Myc is downstream of KRAS and can be involved in the regulation of multiple oncogenic pathways and signaling pathways in pancreatic cancer. Over expressing of C-Myc promotes glycolysis and glutamine uptake in pancreatic cancer cells, promotes cell metabolism and proliferation, is an important factor driving the progress and maintenance of pancreatic cancer, and is related to chemotherapy and immunotherapy drug resistance. C-Myc also interacts with cell cyclin-dependent kinase(CDK) and non-coding RNA to regulate the proliferation, development and metastasis of pancreatic cancer. Therefore, targeting C-Myc was regarded as an effective strategy for the treatment of pancreatic cancer. The activation of C-Myc depends on heterodimerization with its partner MAX and thereby paly a role through binding to the canonical E-Box sequence 5’-CACGTG-3’. Researches showed direct targeting of C-Myc can inhibit the growth of pancreatic carcinoma,such as promoting the degradation of C-Myc, inhibiting the binding of C-Myc/MAX and blocking the binding of C-Myc/MAX to E-box. However, direct targeting has been proved challenging because of its special protein structure. Indirect targeting of C-Myc provided a new strategy for the treatment of pancreatic cancer. C-Myc can be indirected targeting through inhibiting transcription and translation of C-Myc, C-Myc-MAX heterodimerization and promote the ubiquitination and degradation of C-Myc, thus affects the occurrence, development and metastasis of pancreatic cancer.