of neuraminidase. During 2003-2004, 29 H9N2 AIV isolates were obtained from different states of India. Subtyping of the virus was carried out by neuraminidase inhibition assay, HI and RT-PCR. On sequencing of HA gene it showed that isolates were very closely related (95- 99.6%). The isolates showed 92-96% homology with other isolates from Asia and Germany. On amino acid sequences it shows that it has a tendency to bind with α 2- 6 sialic acid receptor (Nagarajan et al., 2009). Four out of six isolates showed glycyosylation at 5 th position in HA1 cleavability. But remaining two showed at 7 th position of glycosylation site. On phylogenetic analysis it showed that it had a resemblance with quail isolate. Twelve H9N2 viruses were isolated in Pakistan in the year 2005-2009. The HA sequences showed that it contain leucine instead of glutamine at position 226 which is a recognized indicator for α 2-6 galactose receptor (Iqbal et al., 2009). The NS gene showed considerable genetic variation. It showed analogy to H5 or H7 subtype rather than H9N2 subtype.
9. Wilkesmann A, Ammann RA, Schildgen O, Eis-Hübinger AM, Müller A, Seidenberg J, Stephan V, Rieger C, Herting E, Wygold T, Hornschuh F, Groothuis JR, Simon A; DSM RSV Ped Study Group. Hospitalized children with respiratory syncytial virus infection and neuromuscular impairment face an increased risk of a complicated course. Pediatr Infect Dis J. 2007 Jun;26(6):485-91.
Human influenza is a seasonal disease associated with significant morbidity and mortality. The most effective means for controlling infection and thereby reducing morbidity and mortality is vaccination with a three inactivated influenzavirus strains mixture, or by intranasal administration of a group of three different live attenuated influenza vaccine strains. Comparing to the inactivated vaccine, the attenuated live viruses allow better elicitation of a long-lasting and broader immune (humoral and cellular) response that represents a naturally occurring transient infection. The cold-adapted (ca) influenza A/AA/6/60 (H2N2) (AA ca) virus is the backbone for the live attenuated trivalent seasonal influenza vaccine licensed in the United States. Similarly, the influenza A components of live-attenuated vaccines used in Russia have been prepared as reassortants of the cold-adapted (ca) H2N2 viruses, A/Leningrad/134/17/57-ca (Len/17) and A/Leningrad/134/ 47/57-ca (Len/47) along with virulent epidemic strains. However, the mechanism of temperature-sensitive attenuation is largely elusive. To understand how modification at genetic level of influenzavirus would result in attenuation of human influenzavirus A/PR/8/34 (H1N1,A/PR8), we investigated the involvement of key mutations in the PB1 and/or PB2 genes in attenuation of influenzavirus in vitro and in vivo. We have demonstrated that a few of residues in PB1 and PB2 are critical for the phenotypes of live attenuated, temperature sensitive influenza viruses by minigenome assay and real-time PCR. The information of these mutation loci could be used for elucidation of mechanism of temperature-sensitive attenuation and as a new strategy for influenza vaccine development.
Antibody profile in response to influenza A(H1N1)pdm09 virus infection with and without seasonal influenza vaccination. When comparing change in titer compared to baseline in the natural infection-group, the greatest increase (fold change) was observed for the homologous antigen, followed by 1918 and the other H1 antigens. Smaller but significant rises in antibody titer were observed for all other antigens except H5- 2004. Subjects with a history of seasonal influenzavirus vaccination showed a significantly higher baseline titer for the historic and recent H1 and H3 influenza antigens, but not for H2 and the avian influenzavirus antigens (Figure 2). The natural infection-group had a greater increase in titer for all antigens than the vaccination group, although the response in the persons with seasonal vaccination history was skewed towards seasonal influ- enza antigens H1-1999 and H1-2007, for which most significant differences in response were observed. No significant interaction between time and former seasonal vaccination was found for any of the antigens in this infection group, adjusted for age and gender. Absence of this above mentioned interaction coincides with a model where the time courses of the titers in both vaccination history subgroups are parallel. (Described in Table S1).
13. Data on vaccination coverage for Latin American countries is limited. Brazil’s influenza vaccination campaigns target persons 65 years of age and older for 1999-2001, and 60 years of age and older in 2002; 74% to 87% of those population subgroups were vaccinated. An increasing number of doses were administered each year, from 7,519,114 doses in 1999 to 11,026,124 in 2002. Uruguay has provided influenza vaccination for seniors since 1996. The 2002 influenza vaccination campaign in Uruguay succeeded in vaccinating 233,346 people among 815,592 people over 55 years old (29%). Although Uruguay used to vaccinate persons 60 years of age and older, the age group was changed to 55 years and older in 2002. Persons of other age groups with risk factors for influenza complications are offered the vaccine as well. Vaccination coverage in Uruguay has fluctuated between 31% and 41% during 1996-2001. Argentina has an influenza vaccination program for seniors since 1993; approximately 4 million doses of influenza vaccine were purchased in the country in 2002. Chile vaccinates persons 65 years of age and older, health personnel, and people with chronic diseases registered in the public health system. Each year, Chile vaccinates approximately one and a half million people, with coverage above 95% among those aged 65 years old and over.
10. Lu S, Zheng Y, Li T, Hu Y, Liu X, Xi X, et al. Clinical findings for early human cases of influenza A(H7N9) virus infection, Shanghai, China. Emerg Infect Dis. 2013;19(7):1142-6. 11. Chen Y, Liang W, Yang S, Wu N, Gao H, Sheng J, et al. Human
The lungs were extensively involved, and bilateral areas of consolidation and/or ground-glass opacities on high- resolution computed tomography (HRCT) were already present 4–9 days after hospital admission caused by H1N1 virus infection. 6 The main pathological changes associated with H1N1 virus infection were diffuse alveolar damage, necrotizing bronchiolitis, and extensive hemorrhage. 7 The mortality rate in Brazil was 70 deaths per 100,000 people. 1 General management of lung involvement in our Institution has been extensively covered. 8-11
The first influenza pandemic of the 21st century was caused by a novel swine-origin H1N1 influenzavirus that emerged in early 2009. This virus is substantially less virulent than the 1918 influenzavirus, but it has the potential to acquire amino acid changes in its viral proteins that would increase its pathogenicity. To prepare for such events and future pandemics, we need to understand the molecular basis of the high-virulence phenotype of the 1918 pandemic virus to help identify virulence factors in other emerging pandemic viruses. Additionally, the fact that more than 97% of the people infected with the 1918 virus survived raises the intriguing possibility of some contribution of host genetics to the consequences of influenza (i.e., survival or death). Thus, it is also important to explore host factors that are involved in resistance or susceptibility to influenzavirus infection. Such information could accelerate the development of new antiviral drugs for prophylaxis and treatment, which are urgently needed given the obstacles to rapid development of an effective vaccine against pandemic influenza.
Several outbreaks in Columbiformes have been reported over the past 30 years in many parts of the world caused by an adapted variant AAvV-1 denominated pigeon paramyxovirus 1 (PPMV-1) (Alexander 2011), which have been described in countries of the South America (Zanetti et al. 2001). These panzootic strains belong to genotype VI, which presents 9 subgenotypes (Dimitrov et al. 2016), and has been previously described in high mortality outbreaks worldwide in different species of birds (Alexander et al. 1985, 1997). Pigeons must be considered seriously as a potential source of NDV infection and disease for commercial poultry flocks (Kommers et al. 2002), and may be subclinically infected, spreading the virus for a considerable period of time without clinical signs (Carrasco et al. 2008, Catroxo et al. 2011). These may consist of apathy, anorexia, weight loss, prostration, diarrhea, polyuria, conjunctivitis, periocular edema, ruffled feathers, sneezing, dyspnea, incoordination, lack of balance, tremors, dehydration, proventricular dilatation, crop emptying problems, leukopenia and death. Some other symptomatic and asymptomatic birds had sudden death (Clavijo et al. 2000, Catroxo et al. 2012). Brazil has the status of free of pathogenic NDV in commercial poultry, and in the suspect of the disease the notification to the official veterinary service in the country is mandatory (Brasil 2007, Orsi et al. 2010).
O vírus influenza pertence à família Orthomyxoviridae. Medindo 80 a 120 nm de diâmetro, apresenta fita única de ácido ribonucleico (RNA), contendo oito segmentos, estes com capacidade de replicação semiautônoma e rearranjos aleatórios. Possui três principais tipos antigênicos – A, B e C – com múltiplos subtipos, destacando-se o tipo A, o mais virulento. Para os tipos A e B, as duas glicoproteínas de membrana que têm importância antigênica são a Hemaglutinina (HA) e a Neuraminidase (NA). Esses antígenos são específicos para cada subtipo e variáveis, sendo utilizados para classificar os subtipos. Anticorpos anti-HA neutralizam a replicação viral e são os principais marcadores de imunidade em humanos. Três principais tipos de HA são frequentes nos vírus influenza A patogênicos em humanos – H1, H2 e H3 – e dois de NA – N1 e N2 - embora outros tipos dessas glicoproteínas possam eventualmente ter importância clínica (1, 2).