As early as 1504, influenza began to mean a "visitation" or "outbreak" of any disease affecting many people in a single place at once. During an outbreak of influenza in 1743 that started in Italy and spread throughout Europe, the word reached the English language and was anglicized in pronunciation. Since the mid-1800s, influenza has also been used to refer to severe colds. The shortened form of the word, "(the) flu", is first attested in 1839 as flue with the spelling flu first attested in 1893. Other names that have been used for influenza include epidemic catarrh, la grippe from French, sweating sickness, and, especially when referring to the 1918 pandemic strain, Spanish fever. Research
Influenza research is wide-ranging and includes efforts to understand how influenza viruses enter hosts, the relationship between influenza viruses and bacteria, how influenza symptoms progress, and what make some influenza viruses deadlier than others. Non-structural proteins encoded by influenza viruses are periodically discovered and their functions are continually under research. Past pandemics, and especially the 1918 pandemic, are the subject of much research to understand flu pandemics. As part of pandemic preparedness, the Global Influenza Surveillance and Response System is a global network of laboratories that monitors influenza transmission and epidemiology. Additional areas of research include ways to improve the diagnosis, treatment, and prevention of influenza. Existing diagnostic methods have a variety of limitations coupled with their advantages. For example, NATs have high sensitivity and specificity but are impractical in under-resourced regions due to their high cost, complexity, maintenance, and training required.
Seropositivity for anti-Ro and anti-La is associated with greater severity and longer duration of disease, and findings of their high abundance from the salivary glands of Sjögrens patients suggests their imperative role in the pathogenesis of SS.Beyond genetics, epigenetic abnormality related to DNA methylation, histone acetylation, or microRNA expression probably has a key role in the pathogenesis of autoimmune diseases, including Sjögrens syndrome, though research in this area is very limited. Environmental triggers
Environmental factors, such as glandular viral infection, could prompt epithelial cells to activate the HLA-independent innate immune system through toll-like receptors. Although a number of infectious, exogenous agents have been implicated in the pathogenesis of Sjögrens syndrome, such as Epstein-Barr virus (EBV), human T-lymphotropic virus 1, and hepatitis C virus, their association with Sjögrens syndrome appears weak. While EBV is present in the salivary glands of normal individuals, a high incidence of EBV reactivation in Sjögrens patients has been reported with increased levels of EBV DNA. This indicates viral reactivation and inability of lymphoid infiltrates to control EBV replication in Sjögrens syndrome, leading to the initiation or perpetuation of an immune response in target organs. Nonetheless,  exactly how reactivation of EBV is induced in lesions of patients with Sjögrens syndrome, and which specific molecular mechanisms are involved in the process of viral reactivation,  remain to be clarified. Inflammation
Epithelial cells in Sjögrens syndrome lesions are active participants in the induction and perpetuation of the inflammatory process.