Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the autumn of 1979 a severe influenza epizootic started among camels in Mongolia (Lvov et al., 1982; Viprosi Virusol. 27, 401-405.) Between 1980 and 1983 13 independent isolates of H1N1 viruses were obtained from diseased camels, which were virtually indistinguishable from the human A/USSR/90/77 strain by serological means. Two hundred and seventy-one samples of camel sera collected between 1978 and 1983 contained antibodies against the human A/USSR/90/77 isolate. After experimental infection of camels with some of these isolates, the animals developed similar symptoms as those found during natural infection: coughing, bronchitis, fever, discharge from nose and eyes. A genetic sequence analysis revealed that among the eight segments (genes) the PB1, HA, and NA genes were almost identical with allelic genes of the USSR/77 strain, and the PB2, PA, NP, M, and NS genes were almost identical with those of the A/PR/8/34 strain.
 ...
PMID:A reassortant H1N1 influenza A virus caused fatal epizootics among camels in Mongolia. 824 79

Influenza viruses represent Orthomyxoviridae family. Spherical virions are 80-120 nm in diameter and have two-layer lipid envelope. The following proteins are coded by 8 or 7 segments of the single-stranded RNA: nucleoprotein (NP), polymerase PB2, PB1 and PA, member protein--M1 and M2, glycoproteins--hemagglutinin (HA) and neuraminidase (NA). HA and NA form spikes on the virion surface. On the basis of antigenic differences there are distinguished three types of influenza virus-A, B and C. Besides, influenza A viruses occur in different subtypes, depending on the features of HA and NA. One of influenza characteristics is its antigenic changeability: antigenic drift and antigenic shift. Infection occurs by droplet route, sometimes through direct contact with infected person or surface. Influenza virus attacks epithelial cells of upper respiratory tract, where replication takes place resulting in the production of approximately 1000 of progeny virions during a single 6-12 h cycle in one cell. Necrosis of ciliary cells of mucosa facilitates invasion of bacterial pathogens. Incubation period lasts on average 1-2 days. Influenza illness without complications characterizes the sudden onset of respiratory symptoms and systemic symptoms. Regression of symptoms usually occurs after 3-5 days, but cough and malaise may be observed for over 2 weeks. Reasons for the severe course of the disease or even death are post-influenza complications, e.g. viral pneumonia and bronchitis, bronchiolitis in children, secondary bacterial pneumonia, otitis media, myocarditis and pericarditis, Reye's syndrome, myositis, myoglobinuria, neurological complications and exacerbation of existing chronic diseases. In the case of influenza there is no possible to make the unquestionable diagnosis only on the basis of clinical picture of the disease. Therefore in some circumstances there is important to make some diagnostic laboratory tests as RT-PCR, immunofluorescence assay or isolation of virus and detection of the specific antibodies. The main determinants of the immunity to influenza virus infection are antihemagglutinin (anti-HA) antibodies and antineuraminidase antibodies (anti-NA). The former play fundamental role for the protection against the infection, while anti-NA antibodies limit virus spreading and contribute to a milder course of the disease. In the response to influenza infection there are observed serum immunoglobulines IgG and IgM (after the first contact with the antigen), while immunoglobulines IgA are produced rarely. The latter are produced locally in the high concentrations on the mucus of respiratory tract. Cellular immunological response is important for recovery from influenza where a significant role of cytotoxic T lymphocytes should be emphasized. These lymphocytes are able to kill infected cells in the earliest phases of replication before the progeny virions are formed.
 ...
PMID:[Various sides of influenza, part I--structure, replication, changeability of influenza viruses, clinical course of the disease, immunological response and laboratory diagnostics]. 1716 90

In October and November 2010, novel H1N2 reassortant influenza viruses were identified from pigs showing mild respiratory signs that included cough and depression. Sequence and phylogenetic analysis showed that the novel H1N2 reassortants possesses HA and NA genes derived from recent H1N2 swine isolates similar to those isolated from Midwest. Compared to the majority of reported reassortants, both viruses preserved human-like host restrictive and putative antigenic sites in their HA and NA genes. The four internal genes, PB2, PB1, PA, and NS were similar to the contemporary swine triple reassortant viruses' internal genes (TRIG). Interestingly, NP and M genes of the novel reassortants were derived from the 2009 pandemic H1N1. The NP and M proteins of the two isolates demonstrated one (E16G) and four (G34A, D53E, I109T, and V313I) amino acid changes in the M2 and NP proteins, respectively. Similar amino acid changes were also noticed upon incorporation of the 2009 pandemic H1N1 NP in other reassortant viruses reported in the U.S. Thus the role of those amino acids in relation to host adaptation need to be further investigated. The reassortments of pandemic H1N1 with swine influenza viruses and the potential of interspecies transmission of these reassortants from swine to other species including human indicate the importance of systematic surveillance of swine population to determine the origin, the prevalence of similar reassortants in the U.S. and their impact on both swine production and public health.
 ...
PMID:Identification of swine H1N2/pandemic H1N1 reassortant influenza virus in pigs, United States. 2239 32