The development of antivirals for respiratory viruses has advanced markedly in response to the growing threat of pathogens such as Influenzavirus (IAV), respiratory syncytial virus (RSV), and SARS-CoV-2. This article reviews the advances and challenges in this field, highlighting therapeutic strategies that target critical stages of the viral replication cycle, including inhibitors of viral entry, replication, and assembly. In addition, innovative approaches such as inhibiting host cellular proteins to reduce viral resistance and repurposing existing drugs are explored, using advanced bioinformatics tools that optimize the identification of antiviral candidates. The analysis also covers emerging technologies such as nanomedicine and CRISPR gene editing, which promise to improve the stability and efficacy of treatments. While current antivirals offer valuable options, they face challenges such as viral evolution and the need for accessible treatments for vulnerable populations. This article underscores the importance of continued innovation in biotechnology to overcome these limitations and provide safe and effective treatments. Combining traditional and advanced approaches in developing antivirals is essential in order to address respiratory viral diseases that affect global health.

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.

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.