In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[Q]: Influenza infection and pneumonia are known to cause much of their mortality by inducing acute respiratory distress syndrome (ARDS), which is the most severe form of acute lung injury (ALI). Angiotensin-converting enzyme 2 (ACE2), which is a negative regulator of angiotensin II in the renin-angiotensin system, has been reported to have a crucial role in ALI. Downregulation of ACE2 is always associated with the ALI or ARDS induced by avian influenza virus, severe acute respiratory syndrome-coronavirus, respiratory syncytial virus and sepsis. However, the molecular mechanism of the decreased expression of ACE2 in ALI is unclear. Here we show that avian influenza virus H5N1 induced the upregulation of miR-200c-3p, which was then demonstrated to target the 3′-untranslated region of ACE2. Then, we found that nonstructural protein 1 and viral RNA of H5N1 contributed to the induction of miR-200c-3p during viral infection. Additionally, the synthetic analog of viral double-stranded RNA (poly (I:C)), bacterial lipopolysaccharide and lipoteichoic acid can all markedly increase the expression of miR-200c-3p in a nuclear factor-κB-dependent manner. Furthermore, markedly elevated plasma levels of miR-200c-3p were observed in severe pneumonia patients. The inhibition of miR-200c-3p ameliorated the ALI induced by H5N1 virus infection in vivo, indicating a potential therapeutic target. Therefore, we identify a shared mechanism of viral and bacterial lung infection-induced ALI/ARDS via nuclear factor-κB-dependent upregulation of miR-200c-3p to reduce ACE2 levels, which leads increased angiotensin II levels and subsequently causes lung injury.
[A]: miRNA-200c-3p is crucial in acute respiratory distress syndrome


[Q]: Background: The influenza A virus subtypes H1N1, H1N2 and H3N2 are the most prevalent subtypes in swine. In 2003, a reassorted H1N2 swine influenza virus (SIV) subtype appeared and became prevalent in Denmark. In the present study, the reassortant H1N2 subtype was characterised genetically and the infection dynamics compared to an "avian-like" H1N1 virus by an experimental infection study. Methods: Sequence analyses were performed of the H1N2 virus. Two groups of pigs were inoculated with the reassortant H1N2 virus and an "avian-like" H1N1 virus, respectively, followed by inoculation with the opposite subtype four weeks later. Measurements of HI antibodies and acute phase proteins were performed. Nasal virus excretion and virus load in lungs were determined by real-time RT-PCR. The phylogenetic analysis revealed that the reassorted H1N2 virus contained a European "avian-like" H1-gene and a European "swine-like" N2-gene, thus being genetically distinct from most H1N2 viruses circulating in Europe, but similar to viruses reported in 2009/2010 in Sweden and Italy. Sequence analyses of the internal genes revealed that the reassortment probably arose between circulating Danish "avian-like" H1N1 and H3N2 SIVs. Infected pigs developed cross-reactive antibodies, and increased levels of acute phase proteins after inoculations. Pigs inoculated with H1N2 exhibited nasal virus excretion for seven days, peaking day 1 after inoculation two days earlier than H1N1 infected pigs and at a six times higher level. The difference, however, was not statistically significant. Pigs euthanized on day 4 after inoculation, had a high virus load in all lung lobes. After the second inoculation, the nasal virus excretion was minimal. There were no clinical sign except elevated body temperature under the experimental conditions. The "avian-like" H1N2 subtype, which has been established in the Danish pig population at least since 2003, is a reassortant between circulating swine "avian-like" H1N1 and H3N2. The Danish H1N2 has an "avian-like" H1 and differs from most other reported H1N2 viruses in Europe and North America/Asia, which have H1-genes of human or "classical-swine" origin, respectively. The variant seems, however, also to be circulating in countries like Sweden and Italy. The infection dynamics of the reassorted "avian-like" H1N2 is similar to the older "avian-like" H1N1 subtype.
[A]: Genetic and biological characterisation of an avian-like H1N2 swine influenza virus generated by reassortment of circulating avian-like H1N1 and H3N2 subtypes in Denmark


[Q]: Transmissible gastroenteritis virus (TGEV) of pigs and porcine epidemic diarrhea virus (PEDV) are two porcine coronaviruses in the genus Alphacoronavirus of the Coronavirinae subfamily in the Coronaviridae family within the order Nidovirales. Based on sequence heterogeneity, PED viruses are tentatively categorized as "classical" and "emerging" strains. The classical strains include PED viruses identified between 1970s to 2010, whereas PED viruses isolated after 2010 are referred to as emerging strains. The emerging strains are further divided into "non-S INDEL (insertions and deletions)" and "S INDEL" strains on the basis of the spike (S) protein sequences and virulence in piglets. Another proposal classifies PED viruses into up to five genotypes. The enveloped virions of coronaviruses are spherical and/or pleomorphic with diameters of 144.8 ± 7.2 nm for TGEV (PUR46-MAD strain) and 95-190 nm for PEDV (CV777 strain). Viral envelope contains the spike (S), membrane (M), and envelope (E) proteins. Homotrimeric S protein complexes form the distinctive "corona-like" structure on the surface of the virions. Within the envelope, there exists a nucleocapsid consisting of the nucleocapsid (N) protein and viral genomic RNA. Both TGEV and PEDV have a typical genomic organization of coronaviruses. The positive-sense, single-stranded RNA genome is approximately 28 kb in length with a 5′ cap structure and a 3′ polyadenylated tail. The coding sequence is flanked by untranslated regions (UTRs) at 5′ and 3′ ends. The N-terminal two-thirds of the genome contain one major open reading frame ORF1a encoding replicase polyprotein pp1a. A -1 frameshift just 5′ to the stop codon of ORF1a gives rise to ORF1b encoding a much longer replicase polyprotein pp1ab. These polyproteins are cleaved into 16 nonstructural proteins (nsps) mostly involved in viral RNA replication. The rest 10-kb genome codes for structural proteins S, M, E, and N, as well as accessory proteins with various functions (Fig. 1) . TGEV encodes three accessory proteins, whereas PEDV encodes one.
[A]:
Transmissible Gastroenteritis Virus of Pigs and Porcine Epidemic Diarrhea Virus