During infection, positive-stranded RNA causes a rearrangement of the host cell membrane, resulting in specialized membrane structure formation aiding viral genome replication. Double-membrane vesicles (DMVs), typical structures produced by virus-induced membrane rearrangements, are platforms for viral replication. Nidoviruses, one of the most complex positive-strand RNA viruses, have the ability to infect not only mammals and a few birds but also invertebrates. Nidoviruses possess a distinctive replication mechanism, wherein their nonstructural proteins (nsps) play a crucial role in DMV biogenesis. With the participation of host factors related to autophagy and lipid synthesis pathways, several viral nsps hijack the membrane rearrangement process of host endoplasmic reticulum (ER), Golgi apparatus, and other organelles to induce DMV formation. An understanding of the mechanisms of DMV formation and its structure and function in the infectious cycle of nidovirus may be essential for the development of new and effective antiviral strategies in the future.

Human livelihood highly depends on applying different sources of energy whose utilization is associated with air pollution. On the other hand, air pollution may be associated with glioblastoma multiforme (GBM) development. Unlike other environmental causes of cancer (e.g., irradiation), air pollution cannot efficiently be controlled by geographical borders, regulations, and policies. The unavoidable exposure to air pollution can modify cancer incidence and mortality. GBM treatment with chemotherapy or even its surgical removal has proven insufficient (100% recurrence rate; patient\'s survival mean of 15 months; 90% fatality within five years) due to glioma infiltrative and migratory capacities. Given the barrage of attention and research investments currently plowed into next-generation cancer therapy, oncolytic viruses are perhaps the most vigorously pursued. Provision of an insight into the current state of the research and future direction is essential for stimulating new ideas with the potentials of filling research gaps. This review manuscript aims to overview types of brain cancer, their burden, and different causative agents. It also describes why air pollution is becoming a concerning factor. The different opinions on the association of air pollution with brain cancer are reviewed. It tries to address the significant controversy in this field by hypothesizing the air-pollution-brain-cancer association via inflammation and atopic conditions. The last section of this review deals with the oncolytic viruses, which have been used in, or are still under clinical trials for GBM treatment. Engineered adenoviruses (i.e., DNX-2401, DNX-2440, CRAd8-S-pk7 loaded Neural stem cells), herpes simplex virus type 1 (i.e., HSV-1 C134, HSV-1 rQNestin34.5v.2, HSV-1 G207, HSV-1 M032), measles virus (i.e., MV-CEA), parvovirus (i.e., ParvOryx), poliovirus (i.e., Poliovirus PVSRIPO), reovirus (i.e., pelareorep), moloney murine leukemia virus (i.e., Toca 511 vector), and vaccinia virus (i.e., vaccinia virus TG6002) as possible life-changing alleviations for GBM have been discussed. To the best of our knowledge, this review is the first review that comprehensively discusses both (i) the negative/positive association of air pollution with GBM; and (ii) the application of oncolytic viruses for GBM, including the most recent advances and clinical trials. It is also the first review that addresses the controversies over air pollution and brain cancer association. We believe that the article will significantly appeal to a broad readership of virologists, oncologists, neurologists, environmentalists, and those who work in the field of (bio)energy. Policymakers may also use it to establish better health policies and regulations about air pollution and (bio)fuels exploration, production, and consumption.

Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically important viruses affecting the swine industry worldwide. MicroRNAs (miRNAs) play vital roles in virus-host interactions by regulating the expression of viral or host gene at posttranscriptional level. Our previous research showed that PRRSV infection down-regulates the expression of heme oxygenase-1 (HO-1), a pivotal cytoprotective enzyme, and overexpression of HO-1 inhibits PRRSV replication. In this study, we demonstrate that host miRNA miR-22 can downregulate HO-1 expression by directly targeting its 3\' untranslated region. Suppression of HO-1 expression by miR-22 facilitates PRRSV replication. This work suggests that PRRSV may utilize cellular miRNA to modify antiviral host factor expression, enabling viral replication, which not only provides new insights into virus-host interactions during PRRSV infection, but also suggests potential therapies for PRRSV infection.