Zika virus (ZIKV) was first discovered in 1947 in Uganda but was not considered a public health threat until 2007 when it found to be the source of epidemic activity in Asia. Epidemic activity spread to Brazil in 2014 and continued to spread throughout the tropical and subtropical regions of the Americas. Despite ZIKV being zoonotic in origin, information about transmission, or even exposure of non-human vertebrates and mosquitoes to ZIKV in the Americas, is lacking. Accordingly, from February 2017 to March 2018, we sought evidence of sylvatic ZIKV transmission by sampling whole blood from approximately 2000 domestic and wild vertebrates of over 100 species in West-Central Brazil within the active human ZIKV transmission area. In addition, we collected over 24,300 mosquitoes of at least 17 genera and 62 species. We screened whole blood samples and mosquito pools for ZIKV RNA using pan-flavivirus primers in a real-time reverse-transcription polymerase chain reaction (RT-PCR) in a SYBR Green platform. Positives were confirmed using ZIKV-specific envelope gene real-time RT-PCR and nucleotide sequencing. Of the 2068 vertebrates tested, none were ZIKV positive. Of the 23,315 non-engorged mosquitoes consolidated into 1503 pools tested, 22 (1.5%) with full data available showed some degree of homology to insect-specific flaviviruses. To identify previous exposure to ZIKV, 1498 plasma samples representing 62 species of domestic and sylvatic vertebrates were tested for ZIKV-neutralizing antibodies by plaque reduction neutralization test (PRNT₉₀). From these, 23 (1.5%) of seven species were seropositive for ZIKV and negative for dengue virus serotype 2, yellow fever virus, and West Nile virus, suggesting potential monotypic reaction for ZIKV. Results presented here suggest no active transmission of ZIKV in non-human vertebrate populations or in alternative vector candidates, but suggest that vertebrates around human populations have indeed been exposed to ZIKV in West-Central Brazil.

Oncoviruses, such as Epstein–Barr virus (EBV), human papillomavirus (HPV), and Kaposi sarcoma-associated herpesvirus (KSHV), have been widely discussed for their oncogenic risk. Initially, the oral cavity was disregarded. In recent years, orientation has shifted to the importance of the oral cavity and cancer-related issues via Handbook 19 titled “Oral Cancer Prevention” by the International Agency for Research on Cancer, the WHO Global Oral Health Status Report 2022, and multiple other actions focused on reducing the oversight of this neglected area. Oncoviruses play a significant role in oral cavity malignancies by establishing persistent infections, evading host immune responses, and inducing cellular transformation through the disruption of normal regulatory pathways. Molecular biology and microbiome research have advanced our understanding of the complex interplay between oncoviruses and oral microbiota, demonstrating how coinfections and dysbiosis can enhance viral oncogenic potential. These findings improve the understanding of virus-induced oral cancers and support the development of novel diagnostic and therapeutic strategies. This narrative review focuses on the relationship between oncoviruses and the oral cavity by focusing on how a specific virus triggers tumorigenesis for each of the described viruses and how it affects oral cavity cancer development. Finally, we describe recent advances and future perspectives including vaccines and/or treatment.

Although chronic hepatitis C has been effectively treated with direct-acting antivirals (DAAs), the use of conventional therapy with peg-interferon (Peg-IFN) or (predominantly) ribavirin (RBV), remains widespread. R70Q/H and L/C91M amino acid substitutions in the hepatitis C virus (HCV) core protein may modulate responses to IFN and/or RBV, and are associated with cirrhosis, hepatocellular carcinoma (HCC), insulin resistance, and liver steatosis. We evaluated the R70Q/H and L/C91M substitutions, clinical and epidemiological profiles, and risk factors of Brazilian patients chronically infected with HCV subgenotypes 1a and 1b (HCV-GT1a and HCV-GT1b) unresponsive to IFN and/or RBV therapy. Sequencing and pyrosequencing analyses and sociodemographic and clinical predictive variables were used to assess the relationship between R70Q/H and L/C91M substitutions. Leukocyte counts, ALT levels, and ALT/AST ratios were significantly reduced in treated individuals, but more of these patients had advanced fibrosis and cirrhosis. L91M was more prevalent (19.7%), occurring only in HCV-GT1b, followed by R70Q/P (11.5%) and R70P (1.4%). R70Q/P exhibited higher mean AST, ALT, and GGT values, whereas L91M showed higher mean GGT values. Pyrosequencing of the L91M position revealed mutant subpopulations in 43.75% of samples.

Background/Objectives: Ulcerative colitis (UC) and Crohn’s disease (CD) are the usual clinical forms of inflammatory bowel disease (IBD). Changes in the oral microbiota, especially the presence of emerging fungi and herpesviruses, have been shown to worsen the clinical aspects of IBD. The aim of this study was to screen for emerging pathogens in the oral yeast microbiota and the presence of herpesvirus in IBD patients. Methods: Oral swabs of seven UC or CD patients were collected. The samples were plated on Sabouraud Dextrose Agar and subcultured on CHROMagar Candida and CHROMagar Candida Plus. Polyphasic taxonomy was applied and identified using molecular tools, such as MALDI-TOF MS and ITS partial sequencing. Multiplex qPCR was used to identify the herpesvirus. Results: The mean age was 38.67 ± 14.06 years, 57.14% were female, and two had diabetes. The CD patients presented with Rhodotorula mucilaginosa, Candida orthopsilosis and Kodamaea jinghongensis, while the UC patients presented with Cutaneotrichosporon dermatis, Candida glabrata, Candida lusitanea and Candida tropicalis. Two UC individuals had at least one herpesvirus. In the first individual, a co-detection of Herpes Simplex Virus 1 (HSV-1) and C. lusitaniae was observed. The second presented with co-infections of Epstein–Barr virus (EBV), Human Herpesvirus 7 (HHV-7) and C. tropicalis. Conclusions: We identified rarely described yeasts and co-infections in IBD patients, highlighting the need to identify emerging pathogens in the oral microbiota, as they may contribute to opportunistic infections.

Colorectal and cervical cancers represent an important public health problem worldwide, particularly in Brazil. Colorectal cancer is one of the most frequently diagnosed malignancies worldwide and the most common cancer in both men and woman in Brazil. Although cervical cancer also remains a significant public health concern in the female population due to its high incidence and mortality rates. Epstein‐Barr virus (EBV), and Polyomaviruses (JCPyV and BKPyV) are considered as oncoviruses with a prevalence of 90% in the adult population. Studies suggest that coinfection with Human papillomavirus (HPV) and EBV, JCPyV and BKPyV can be associated with anal cancer, with HPV being the dominant viral cause. Although in cervical cancer, this coinfection is often observed, and it may enhance cervical oncogenic potential. These facts are particularly concerning in women living with HIV, who are more susceptible to persistent HPV infections and HPV‐related cancers. This study aimed to investigate EBV, JCPyV and BKPyV presence in HPV‐infected women living with HIV. This cross‐sectional study collected 33 cervical and 30 anal scrapings samples, as well as 26 paired samples from both sites from HPV‐positive women living with HIV. Viral detection and quantification for EBV, JCPyV and BKPyV were performed using real‐time polymerase chain reaction (qPCR), while HPV detection and genotyping utilized the Novaplex ^TM assay. EBV was detected in 33.3% of anal scraping and 21.2% in cervical scraping. HPV 51 and HPV 56 were most frequently detected in anal and cervical scrapings, respectively. The EBV mean viral load was higher in cervical scraping (2.27 × 10^5 copies/mL) when compared to anal scraping (1.19 × 10^5 copies/mL) in relation of JCPyV and BKPyV viral loads. Regarding coinfections, it was found that EBV presented a high coinfection rate with high‐risk HPV genotypes (hrHPV) (14.6%) with HPV 31 in both samples. This study provided valuable data about the frequency of EBV in anal and cervical HPV‐positive women. The elevated viral load of EBV in cervical scrapings may suggest a potential role in modulating the local microenvironment and warrants further investigation into the synergistic effects of EBV and HPV in anogenital and cervical carcinogenesis. Overall, the results of this study emphasize the need for further investigation into the role of these viruses in the progression of cervical lesions.

Human populations are classified as secretors or non-secretors by, respectively, the ability to produce or not produce FUT2 enzyme (alpha-1,2-fucosyltransferase; FUT2 gene). Non-secretors have some protection against diseases and viral infections. Two single-nucleotide polymorphisms (SNPs), rs601338 (non-secretor; sese), and rs1047781 (weak secretor; Se^w), are known population markers. In this study, 68 saliva samples collected from children living in the Brazilian Amazon region were evaluated for zygosity—genotyping (homozygous or heterozygous) of the rs601338 and rs1047781 SNPs by pyrosequencing. Nine children were heterozygous (Sese) for the rs601338 SNP (13.2%; 9/68) and one homozygous (sese) (1.5%; 1/68). One child that was heterozygous for the rs601338 SNP was also heterozygous for the rs1047781 SNP (Se^w) (1.5%; 1/68). By using Sanger nucleotide sequencing of the FUT2 coding region, strongly linked SNPs (171A>G, 216C>T, 357T>C, 428G>A, 739G>A, 960A>G), including the FUT2*01N.02 allele (428G>A; 739A>G), were detected and have been associated with non-secretor children. A novel SNP (315C>T) and others (40A>G; 480C>T; 863C>T) detected in worldwide populations were also detected. The sensitivity of the pyrosequencing method provided an unprecedented discovery of the zygosity of the SNP rs1047781 only previously detected in East and Southeast Asians. The identification of novel SNPs in this population expands our knowledge of genetic susceptibility to viral infections.