Search

Zika (ZIKV) and Chikungunya (CHIKV) viruses are mosquito-transmitted infections, or vector-borne pathogens, that emerged a few years ago. Reliable diagnostic tools for ZIKV and CHIKV—inexpensive, multiplexed, rapid, highly sensitive, and specific point-of-care (POC) systems—are vital for appropriate risk management and therapy. We recently studied a detection system with great success in Mexico (Villahermosa, state of Tabasco), working with human sera from patients infected with those viruses. The research conducted in Mexico validated the efficacy of a novel two-step rapid isothermal amplification technique (RAMP). This approach, which encompasses recombinase polymerase amplification (RPA) followed by loop-mediated isothermal amplification (LAMP), had been previously established in the lab using lab-derived Zika (ZIKV) and Chikungunya (CHIKV) viruses. Crucially, our findings confirmed that this technique is also effective when applied to human sera samples collected from locally infected individuals in Mexico.

In mammals, the placenta is a connection between a mother and a new developing organism. This tissue has a protective function against some microorganisms, transports nutrients, and exchanges gases and excretory substances between the mother and the fetus. Placental tissue is mainly composed of chorionic villi functional units called trophoblasts (cytotrophoblasts, the syncytiotrophoblast, and extravillous trophoblasts). However, some viruses have developed mechanisms that help them invade the placenta, causing various conditions such as necrosis, poor perfusion, and membrane rupture which, in turn, can impact the development of the fetus and put the mother’s health at risk. In this study, we collected the most relevant information about viral infection during pregnancy which can affect both the mother and the fetus, leading to an increase in the probability of vertical transmission. Knowing these mechanisms could be relevant for new research in the maternal–fetal context and may provide options for new therapeutic targets and biomarkers in fetal prognosis.

Human Adenoviruses are a diverse family of viruses that can infect a variety of tissues causing acute or persistent infection. Viruses induce numerous cellular alterations as they hijack cellular functions to promote viral progeny. Recent research has shed light on the functions of viral proteins in orchestrating viral production, revealing that many of these functions overlap with oncogenesis or metabolic disruption. Studies of the Adenovirus family (Adenoviridae) have identified oncogenic members, such as Adenovirus (Ad-)2, 5, 9, and 12, and also Ad-36, which is most extensively studied for its ability to induce metabolic alterations. Specifically, Adenoviruses encode a gene product known as early region 4 open reading frame 1 (E4orf1), which has emerged as an oncoprotein and regulator of metabolism depending on the lineage of the infected host cell. This article aims to provide insight into the functions of the viral protein E4orf1 and the overlapping similarities between the oncogenic process and cell metabolism.

Gastric cancer is the third cause of cancer death worldwide and infection by Helicobacter pylori (H. pylori) is considered the most important risk factor, mainly by the activity of its virulence factor CagA. H. pylori/CagA-induced chronic inflammation triggers a series of gastric lesions of increased severity, starting with gastritis and ending with cancer. IL-1β has been associated with tumor development and invasiveness in different types of cancer, including gastric cancer. Currently, it is not clear if there is an association between CagA and IL-1β at a cellular level. In this study, we analyzed the effects of IL-1β and CagA on MCF-10A nontransformed cells. We found evidence that both CagA and IL-1β trigger the initiation of the epithelial-to-mesenchymal transition characterized by β-catenin nuclear translocation, increased expression of Snail1 and ZEB1, downregulation of CDH1, and morphological changes during MCF-10A acini formation. However, only CagA induced MMP9 activity and cell invasion. Our data support that IL-1β and CagA target the β-catenin pathway, with CagA leading to acquisition of a stage related to aggressive tumors.

Zika virus is a mosquito-borne viral disease that emerged as a significant health problem in the Americas after an epidemic in 2015. Especially concerning are cases where Zika is linked to the development of brain abnormalities in newborns. Unlike other flaviviruses, Zika can be transmitted sexually, increasing the potential for intraspecies infection. Several reports show that the virus can persist for months in the testis of males after clearance of viremia, and that females are highly susceptible to infection via sexual transmission. The most common route of sexual transmission is male-to-female, which suggests that the mechanism driving persistence of Zika in the testis is essential for dissemination. The immune system plays an essential role in Zika infection. In females, a robust response inhibits the virus to control the infection. In males, however, the immunological response to Zika infection correlates with viral persistence. Thus, the immune system may have a dual role in sexually transmitted pathogenesis. The mechanism by which the immune system allows the virus to enter an immune-privileged site while continuing to disseminate is unclear. In this mini-review, we highlight advances in our knowledge of sexually transmitted Zika virus pathogenesis and the possible mechanisms mounted by the immune system that control or exacerbate the infection.