As amostras foram agrupadas em BVDV-1 (11/19), BVDV-2 (6/19) e num terceiro grupo de amostras denominadas "atípicas" (2/ 19). Das onze amostras genotipadas como BVDV-1, oito amostras foram sub-genotipadas como BVDV-1a, enquanto que a maioria (4/6) das amostras de BVDV-2 foi agrupada como BVDV2b. Duas amostras provenientes de fetos bovinos abortados foram classificadas como atípicas, não BVDV-1 e 2. A presença da diversidade genética de BVDV detectada nas amostras estudadas pode ser responsável por falhas vacinais e de diagnóstico e deve influenciar nas estratégias de controle do BVDV aplicadas nas diferentes regiões brasileiras.TERMOS DE INDEXAÇÃO: BVDV-1, BVDV-2, Pestivirus, Brazil, análise filogenética. INTRODUCTION INTRODUCTION INTRODUCTION INTRODUCTION INTRODUCTIONInfections of cattle by bovine viral diarrhea virus (BVDV) are widespread cause of major economic losses to the cattle industry (Houe 1999). Clinical symptoms may involve the reproductive, respiratory, immune, and gastrointestinal systems, with signs that may range from disease with high mortality rates to asymptomatic infections. The latter is observed in most cases (Pellerin et al. 1994, Ridpath et al.1994, Baker 1995, Fray et al. 2000.BVDV is an enveloped RNA virus that belongs to family Flaviviridae, genus Pestivirus. The viral positive single stranded genome of approximately 12.5 kb in size contains a single open reading frame (ORF) flanked by two non-translating terminal regions, named 5' and 3'-UTR. The single ORF is directly translated and gives rise to a long polyprotein which is co-translationally cleaved, originating 10 to 12 mature viral proteins (Collet et al. 1988, Meyer et al. 1989.Isolates have been subdivided in genotypes BVDV-1 and BVDV-2. These were further split into subgenotypes.

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BackgroundPCV2 has emerged as one of the most devastating viral infections of swine farming, causing a relevant economic impact due to direct losses and control strategies expenses. Epidemiological and experimental studies have evidenced that genetic diversity is potentially affecting the virulence of PVC2. The growing number of PCV2 complete genomes and partial sequences available at GenBank questioned the accepted PCV2 classification.MethodsNine hundred seventy five PCV2 complete genomes and 1,270 ORF2 sequences available from GenBank were subjected to recombination, PASC and phylogenetic analyses and results were used for comparison with previous classification scheme.ResultsThe outcome of these analyses favors the recognition of four genotypes on the basis of ORF2 sequences, namely PCV2a, PCV2b, PCV2c and PCV2d-mPCV2b. To deal with the difficulty of founding an unambiguous classification and accounting the impossibility to define a p-distance cut-off, a set of reference sequences that could be used in further phylogenetic studies for PCV2 genotyping was established. Being aware that extensive phylogenetic analyses are time-consuming and often impracticable during routine diagnostic activity, ORF2 nucleotide positions adequately conserved in the reference sequences were identified and reported to allow a quick genotype differentiation.ConclusionsGlobally, the present work provides an updated scenario of PCV2 genotypes distribution and, based on the limits of the previous classification criteria, proposes new rapid and effective schemes for differentiating the four defined PCV2 genotypes.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-015-0361-x) contains supplementary material, which is available to authorized users.

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Porcine epidemic diarrhea virus strains from the G1b cluster are considered less pathogenic compared to the G2b cluster. The aim of this study was to compare the ability of G1b-based live virus exposure against use of a commercial G2b–based inactivated vaccine to protect growing pigs against G2b challenge. Thirty-nine PEDV naïve pigs were randomly divided into five groups: EXP-IM-1b (intramuscular G1b exposure; G2b challenge), EXP-ORAL-1b (oral G1b exposure; G2b challenge), VAC-IM-2b (intramuscular commercial inactivated G2b vaccination; G2b challenge), POS-CONTROL (sham-vaccination; G2b challenge) and NEG-CONTROL (sham-vaccination; sham-challenge). Pigs were vaccinated/exposed at 3 weeks of age (day post-vaccination 0, dpv 0), VAC-IM-2b pigs were revaccinated at dpv 14, and the pigs were challenged at dpv 28. Among all groups, VAC-IM-2b pigs had significantly higher anti-PEDV IgG levels on dpv 21 and 28 while EXP-ORAL-1b pigs had significantly higher anti-PEDV IgA levels on dpv 14, 21, 28 and 35. EXP-ORAL-1b also had detectable IgA in feces. Intramuscular PEDV exposure did not result in a detectable antibody response in EXP-IM-1b pigs. The fecal PEDV RNA levels in VAC-IM-2b pigs were significantly lower 5–7 days after challenge compared to the POS-CONTROL group. Under the study conditions a commercial inactivated G2b-based vaccine protected pigs against G2b challenge, as evidenced by reduction of PEDV RNA in feces for 3–4 logs during peak shedding and a shorter viral shedding duration. The oral, but not the intramuscular, experimental G1b-based live virus exposure induced a high anti-PEDV IgA response prior to challenge, which apparently did not impact PEDV shedding compared to POS-CONTROL pigs.