Comparison of the Immunogenicity and Safety of Two Pediatric TBE Vaccines Based on the Far Eastern and European Virus SubtypesRead the full article
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Analysis of Nucleotide Alterations in the E6 Genomic Region of Human Papillomavirus Types 6 and 11 in Condyloma Acuminatum Samples from Brazil
Condyloma acuminata (CA), or genital warts, are benign proliferative epidermal or mucous lesions that are caused by infection with human papillomavirus (HPV), mainly the low-risk types 6 and 11. HPV variants are defined as viral sequences that share identity in the nucleotide sequence of the L1 gene greater than 98%. Based on this criterion, HPV6 and 11 variant lineages have been studied, and there are ongoing attempts to correlate these genetic variants with different clinical findings of infection. Therefore, the aims of this study were to detect variants and nucleotide alterations present in the E6 regions of HPV types 6 and 11 found in CA samples, to correlate the HPV presence with the clinical-pathological data of the patients, and to determine phylogenetic relationships with variants from other places in the world. The E6 regions of 25 HPV6 samples and 7 HPV11 samples from CA were amplified using PCR with specific primers. The products were ligated to a cloning vector and five colonies of each sample were sequenced to observe the nucleotide alterations. Twelve samples were identified as the HPV6B3 variant, presenting the mutation (guanine) G474A (adenine), and one of them also showed the mutation (thymine) T369G. The other 13 patients were positive for HPV6B1 without nucleotide alterations. In the analysis of the HPV11 samples, all patients showed the mutations T137C and (cytosine) C380T. One patient also presented the nucleotide alteration T410C. None of the mutations found in the 32 analyzed samples resulted in amino acid changes. Patient age, local occurrence, and HIV infection did not show significant association with HPV infection. Besides, the data found in this study did not show a relationship with the geographical region of isolation when compared to other data from different regions of the world. In this way, despite the nucleotide alterations found, it was not possible to observe amino acid changes and variants grouping according to geographical region.
Molecular Characterization of African Swine Fever Viruses from Outbreaks in Peri-Urban Kampala, Uganda
African swine fever (ASF) is an infectious transboundary disease of domestic pigs and wild swine and is currently the most serious constraint to piggery in Uganda. The causative agent of ASF is a large double-stranded linear DNA virus with a complex structure. There are twenty-four ASFV genotypes described to date; however, in Uganda, only genotypes IX and X have been previously described. Inadequate ASF outbreak investigation has contributed to the delayed establishment of effective interventions to aid the control of ASF. Continuous virus characterization enhances the understanding of ASF epidemiology in terms of viral genome variations, extent, severity, and the potential source of the viruses responsible for outbreaks. We collected samples from pigs that had died of a hemorrhagic disease indicative of ASF. DNA was extracted from all samples and screened with the OIE recommended diagnostic PCR for ASF. Partial B646L (p72), full-length E183L (p54) genes, and CVR region of the P72 gene were amplified, purified, and sequenced. Web-based BLAST and MEGA X software were used for sequence analysis. ASF was confirmed in 10 of the 15 suspected pig samples. Phylogenetic analysis confirmed circulation of genotype IX by both full-length E183 (p54) and partial B646L (p72) gene sequencing. Intragenotypic resolution of the CVR region revealed major deletions in the virus genome, in some isolates of this study. The marked reduction in the number of tetrameric tandem repeats in some isolates of this study could potentially play a role in influencing the virulence of this particular genotype IX in Uganda.
Epstein-Barr Virus- (EBV-) Immortalized Lymphoblastoid Cell Lines (LCLs) Express High Level of CD23 but Low CD27 to Support Their Growth
Epstein-Barr virus (EBV) is one of the common human herpesvirus types in the world. EBV is known to infect more than 95% of adults in the world. The virus mainly infects B lymphocytes and could immortalize and transform the cells into EBV-bearing lymphoblastoid cell lines (LCLs). Limited studies have been focused on characterizing the surface marker expression of the immortalized LCLs. This study demonstrates the generation of 15 LCLs from sixteen rheumatoid arthritis (RA) patients and a healthy volunteer using B95-8 marmoset-derived EBV. The success rate of LCL generation was 88.23%. All CD19+ LCLs expressed CD23 (16.94-58.9%) and CD27 (15.74-80.89%) on cell surface. Our data demonstrated two distinct categories of LCLs (fast- and slow-growing) (p<0.05) based on their doubling time. The slow-growing LCLs showed lower CD23 level (35.28%) compared to fast-growing LCLs (42.39%). In contrast, the slow-growing LCLs showed higher percentage in both CD27 alone and CD23+CD27+ in combination. Overall, these findings may suggest the correlations of cellular CD23 and CD27 expression with the proliferation rate of the generated LCLs. Increase expression of CD23 may play a role in EBV immortalization of B-cells and the growth and maintenance of the EBV-transformed LCLs while CD27 expression might have inhibitory effects on LCL proliferation. Further investigations are warranted to these speculations.
Poly-ADP Ribosyl Polymerase 1 (PARP1) Regulates Influenza A Virus Polymerase
Influenza A viruses (IAV) are evolutionarily successful pathogens, capable of infecting a number of avian and mammalian species and responsible for pandemic and seasonal epidemic disease in humans. To infect new species, IAV typically must overcome a number of species barriers to entry, replication, and egress, even while virus replication is counteracted by antiviral host factors and innate immune mechanisms. A number of host factors have been found to regulate the replication of IAV by interacting with the viral RNA-dependent RNA polymerase (RdRP). The host factor PARP1, a poly-ADP ribosyl polymerase, was required for optimal functions of human, swine, and avian influenza RdRP in human 293T cells. In IAV infection, PARP1 was required for efficient synthesis of viral nucleoprotein (NP) in human lung A549 cells. Intriguingly, pharmacological inhibition of PARP1 enzymatic activity (PARylation) by 4-amino-1,8-naphthalimide led to a 4-fold increase in RdRP activity, and a 2.3-fold increase in virus titer. Exogenous expression of the natural PARylation inhibitor PARG also enhanced RdRP activity. These data suggest a virus-host interaction dynamic where PARP1 protein itself is required, but cellular PARylation has a distinct suppressive modality, on influenza A viral polymerase activity in human cells.
Peste Des Petits Ruminants (PPR) in Dromedary Camels and Small Ruminants in Mandera and Wajir Counties of Kenya
A study was conducted to determine the presence of Peste des petits ruminants (PPR) in camel population kept together with small ruminants in Isiolo, Mandera, Marsabit, and Wajir counties of Kenya. This was done in the wake of a disease with unknown etiology “Camel Sudden Death Syndrome” camels in the horn of Africa. Thirty-eight (38) samples, 12, 8, 15, and 3 samples, were collected from Mandera, Wajir, Isiolo, and Marsabit, respectively, from 25 camels, 7 goats, and 4 sheep. One camel in Mandera and one goat in Wajir were confirmed positive for PPR virus (PPRV) through reverse Polymerase Chain Reaction. The analysis of sequences revealed closest nucleotide identities of obtained sequences from both goat and camel to the lineage III of PPRV albeit with 60.29% of nucleotide identity. This study establishes that camels in the study area suffer with PPR manifest clinical signs that are mainly characterized by inappetence, loss of body condition, and general weakness terminally leading to diarrhea, conjunctivitis, and ocular nasal discharges preceding death. These clinical signs are similar to those observed in small ruminants with slight variations of manifestations such as keratoconjunctivitis as well as edema of the ventral surface of the abdomen. This shows that camels could be involved in the epidemiology of PPR in the region and that PPRV could be involved in the epidemics of Camel Sudden Death syndrome. There is therefore a need for resources to be dedicated in understanding the role camels play in the epidemiology of PPR and the role of the disease in Camels Sudden death syndrome.
Genetic Diversity and Phylogenetic Analysis of Citrus tristeza virus Isolates from Turkey
The presence of Citrus tristeza virus (CTV) in Turkey has been known since the 1960s and the virus was detected in all citrus growing regions of the country. Even though serological and biological characteristics of CTV have been studied since the 1980s, molecular characteristics of CTV isolates have not been studied to date in Turkey. In this study, molecular characteristics of 15 CTV isolates collected from different citrus growing regions of Turkey were determined by amplification, cloning, and sequencing of their major coat protein (CP) genes. The sequence analysis showed that the CP genes were highly conserved among Turkish isolates. However, isolates from different regions showed more genetic variation than isolates from the same region. Turkish isolates were clustered into three phylogenetic groups showing no association with geographical origins, host, or symptoms induced in indicator plants. Phylogenetic analysis of Turkish isolates with isolates from different citrus growing regions of the world including well-characterized type isolates of previously established strain specific groups revealed that some Turkish isolates were closely related to severe quick decline or stem pitting isolates. The results demonstrated that although CTV isolates from Turkey are considered biologically mild, majority of them contain severe components potentially causing quick decline or stem pitting.