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Monkeypox virus (MPXV) is a zoonotic pathogen that causes mpox (formerly monkeypox), a febrile rash disease, in humans. It has caused multiple outbreaks in the past (1) but recently acquired [...]

Influenza viruses cause a potentially fatal, highly contagious respiratory disease. Influenza A virus subtypes H1N1 and H3N2, and both lineages of the influenza B virus have affected the Mexican population. The present study aimed to determine the epidemiological characteristics of influenza infections in Northern Mexico during five flu seasons and determines the risk factors for hospitalization. For this purpose, 3,482 patients with confirmed influenza infection tested at the Public Health State Laboratory of Nuevo León using reverse transcription-quantitative PCR from October, 2009 to December, 2014 were evaluated. Patient demographics and clinical characteristics were determined, and data were collected and analyzed. Pandemic influenza A H1N1 subtype was responsible for 52% of the cases in the present study; the influenza A H3N2 subtype was responsible for 27% of cases and the influenza B virus for 12% of cases. In total, 75% of the patients (n=2,611) received ambulatory treatment and 25% (n=871) were hospitalized. The number of hospitalized patients varied across the different seasons analyzed. A greater number of comorbidities were observed in hospitalized patients than the ambulatory patients; 64% of patients with chronic obstructive pulmonary disease (COPD), 60% of patients with chronic kidney disease, and 51% of patients with diabetes were hospitalized. Of the total number of vaccinated patients, only 18% were hospitalized, in contrast to 27% of unvaccinated patients. On the whole, the present study describes the influenza cases identified in the metropolitan area of Monterrey, Mexico. The median age and clinical characteristics of the patients varied according to the season with increasing age, and the presence of dyspnea, polypnea, cyanosis, malaise, COPD, diabetes, or no vaccination, were associated with an increased risk of hospitalization. This clinical characterization becomes relevant as coronavirus 2019 spreads worldwide, rendering its differential diagnosis necessary in respiratory diseases that usually lead to hospitalization, such as influenza. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is one of the leading causes of death in women worldwide. A major challenge in BC is chemoresistance, which is often modulated by epigenetic regulators such as long non-coding RNAs (lncRNAs). Because these regulator lncRNAs may play diverse roles, determining their specific pathways and/or functions is crucial to identify possible biomarkers and/or therapeutic targets for BC. In this study, we used gene expression microarrays in order to identify lncRNAs related to the BC biology. We found, among six differentially expressed (DE) lncRNAs, that the expression of lnc-ERP44-3:6 was consistently down-regulated in all breast tumor tissues compared to normal adjacent tissues of BC patients from northeastern Mexico. Since the role of lnc-ERP44-3:6 remains unknown in BC, we induced its transient overexpression in three different BC cell lines (i.e., MCF10A, MCF-7, and HCC1395) by transfection in order to elucidate its potential downstream effects. Remarkably, our results showed a significant increase in cell death and chemosensitivity to cisplatin at 48 h post-transfection (p < 0.01). In addition, we observed that GAPDH and FAS were up-regulated following the overexpression of lnc-ERP44-3:6. As GAPDH and FAS promote apoptosis in cancer, our findings suggest that the lnc-ERP44-3:6 overexpression induces cell death possibly via up-regulation of one or both genes in BC cell lines. To the best of our knowledge, this is the first study evaluating the overexpression of lnc-ERP44-3:6 and providing insights about its role in BC cells, which suggests that this lncRNA may be an interesting candidate as a potential therapeutic target for BC in our population. However, further studies would be needed to clarify the mechanisms by which an overexpression of lnc-ERP44-3:6 causes both cell death and chemosensitivity to cisplatin. [ABSTRACT FROM AUTHOR]

Abstract Background Several viruses with known oncogenic potential infect prostate tissue, among these are the polyomaviruses BKV, JCV, and SV40; human papillomaviruses (HPVs), and human cytomegalovirus (HCMV) infections. Recently, the Xenotropic Murine Leukemia Virus-related gammaretrovirus (XMRV) was identified in prostate tissue with a high prevalence observed in prostate cancer (PC) patients homozygous for the glutamine variant of the RNASEL protein (462Q/Q). Association studies with the R462Q allele and non-XMRV viruses have not been reported. We assessed associations between prostate cancer, prostate viral infections, and the RNASEL 462Q allele in Mexican cancer patients and controls. Methods 130 subjects (55 prostate cancer cases and 75 controls) were enrolled in the study. DNA and RNA isolated from prostate tissues were screened for the presence of viral genomes. Genotyping of the RNASEL R462Q variant was performed by Taqman method. Results R/R, R/Q, and Q/Q frequencies for R462Q were 0.62, 0.38, and 0.0 for PC cases and 0.69, 0.24, and 0.07 for controls, respectively. HPV sequences were detected in 11 (20.0%) cases and 4 (5.3%) controls. XMRV and HCMV infections were detected in one and six control samples, respectively. The risk of PC was significantly increased (Odds Ratio = 3.98; 95% CI: 1.17-13.56, p = 0.027) by infection of the prostatic tissue with HPV. BKV, JCV, and SV40 sequences were not detected in any of the tissue samples examined. Conclusions We report a positive association between PC and HPV infection. The 462Q/Q RNASEL genotype was not represented in our PC cases; thus, its interaction with prostate viral infections and cancer could not be evaluated.

Halloysite is an aluminosilicate clay that has been widely used for controlled drug delivery, immobilization of enzymes, and for the capture of circulating tumor cells (CTCs). Surface modification of halloysite by organosilanes has been explored to improve their properties. In this study halloysite clay nanotubes (HNTs) were functionalized by two different organosilanes: Trimethoxy(propyl)silane (TMPS), and Triethoxy(octyl)silane (EOS). Untreated and modified samples were characterized by scanning electron microscopy (SEM), X-ray diffractometry (XRD), thermogravimetrical analysis (TGA), and Fourier transform infrared spectroscopy (FTIR). Results showed a strong interaction of organosilanes with the chemical groups present in HNTs. Biocompatibility and cytotoxicity of these nanomaterials were determined using C6 rat glioblastoma cells. Our results indicate that prior to functionalization, HNTs show a high biocompatibility and low cytotoxicity. However, HNTs functionalized with EOS and TMPS showed high cytotoxicity by inducing apoptosis. These results allow the identification of potential applications in biomedical areas for HNTs. [ABSTRACT FROM AUTHOR]

Background: Several viruses with known oncogenic potential infect prostate tissue, among these are the polyomaviruses BKV, JCV, and SV40; human papillomaviruses (HPVs), and human cytomegalovirus (HCMV) infections. Recently, the Xenotropic Murine Leukemia Virus-related gammaretrovirus (XMRV) was identified in prostate tissue with a high prevalence observed in prostate cancer (PC) patients homozygous for the glutamine variant of the RNASEL protein (462Q/Q). Association studies with the R462Q allele and non-XMRV viruses have not been reported. We assessed associations between prostate cancer, prostate viral infections, and the RNASEL 462Q allele in Mexican cancer patients and controls. Methods: 130 subjects (55 prostate cancer cases and 75 controls) were enrolled in the study. DNA and RNA isolated from prostate tissues were screened for the presence of viral genomes. Genotyping of the RNASEL R462Q variant was performed by Taqman method. Results: R/R, R/Q, and Q/Q frequencies for R462Q were 0.62, 0.38, and 0.0 for PC cases and 0.69, 0.24, and 0.07 for controls, respectively. HPV sequences were detected in 11 (20.0%) cases and 4 (5.3%) controls. XMRV and HCMV infections were detected in one and six control samples, respectively. The risk of PC was significantly increased (Odds Ratio = 3.98; 95% CI: 1.17-13.56, p = 0.027) by infection of the prostatic tissue with HPV. BKV, JCV, and SV40 sequences were not detected in any of the tissue samples examined. Conclusions: We report a positive association between PC and HPV infection. The 462Q/Q RNASEL genotype was not represented in our PC cases; thus, its interaction with prostate viral infections and cancer could not be evaluated. [ABSTRACT FROM AUTHOR]

Chikungunya fever is an arthropod-borne infection caused by Chikungunya virus (CHIKV). Even though clinical features of Chikungunya fever in the Mexican population have been described before, there is no detailed information. The aim of this study was to perform a full description of the clinical features in confirmed Chikungunya-infected patients and describe the molecular epidemiology of CHIKV. We evaluated febrile patients who sought medical assistance in Tapachula, Chiapas, Mexico, from June through July 2015. Infection was confirmed with molecular and serological methods. Viruses were isolated and the E1 gene was sequenced. Phylogeny reconstruction was inferred using maximum-likelihood and maximum clade credibility approaches. We studied 52 patients with confirmed CHIKV infection. They were more likely to have wrist, metacarpophalangeal, and knee arthralgia. Two combinations of clinical features were obtained to differentiate between Chikungunya fever and acute undifferentiated febrile illness. We obtained 10 CHIKV E1 sequences that grouped with the Asian lineage. Seven strains diverged from the formerly reported. Patients infected with the divergent CHIKV strains showed a broader spectrum of clinical manifestations. We defined the complete clinical features of Chikungunya fever in patients from Southeastern Mexico. Our results demonstrate co-circulation of different CHIKV strains in the state of Chiapas. [ABSTRACT FROM AUTHOR]

Arboviruses are responsible for several emerging and re-emerging infectious diseases, with dengue, Zika virus disease and Chikungunya fever being the most important arboviral diseases nowadays. Infection of these viruses depends primarily on its ability to replicate and disseminate in mosquitoes. Since these viruses are enveloped, viral replication, assembly and release occurs in the cellular membranes, which depends on the manipulation of host lipid metabolism. Specifically in mammalian cells replication, they use host lipids to establish a compartment known as replication complex that contains the replicase complex. This complex includes viral RNA, proteins and host factors necessary for a successful replication in mammalian cells. Although little is known about extrinsic factor(s) needed for arbovirus replication in vectors,recent reports show that high lipid concentrations are related with increased viral replication in mosquito cells infected with dengue, Zika and Chikungunya viruses. Here, we present a review that focuses on the cellular mechanisms and the lipid environment alteration in mosquito vector after arbovirus infection and their relationship with arbovirus replication., Competing Interests: None

Hepatitis C virus (HCV) replication is associated with the endoplasmic reticulum, where the virus can induce cellular stress. Oxidative cell damage plays an important role in HCV physiopathology. Oxidative stress is triggered when the concentration of oxygen species in the extracellular or intracellular environment exceeds antioxidant defenses. Cells are protected and modulate oxidative stress through the interplay of intracellular antioxidant agents, mainly glutathione system (GSH) and thioredoxin; and antioxidant enzyme systems such as superoxide dismutase, catalase, GSH peroxidase, and heme oxygenase-1. Also, the use of natural and synthetic antioxidants (vitamin C and E, N-acetylcysteine, glycyrrhizin, polyenylphosphatidyl choline, mitoquinone, quercetin, S-adenosylmethionine and silymarin) has already shown promising results as co-adjuvants in HCV therapy. Despite all the available information, it is not known how different agents with antiviral activity can interfere with the modulation of the cell redox state induced by HCV and decrease viral replication. This review describes an evidence-based consensus on molecular mechanisms involved in HCV replication and their relationship with cell damage induced by oxidative stress generated by the virus itself and cell antiviral machinery. It also describes some molecules that modify the levels of oxidative stress in HCV-infected cells.