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In order to multiply and cause disease a virus must transport its genome from outside the cell into the cytosol, most commonly achieved through the endocytic network. Endosomes transport virus particles to specific cellular destinations and viruses exploit the changing environment of maturing endocytic vesicles as triggers to mediate genome release. Previously we demonstrated that several bunyaviruses, which comprise the largest family of negative sense RNA viruses, require the activity of cellular potassium (K.sup.+) channels to cause productive infection. Specifically, we demonstrated a surprising role for K.sup.+ channels during virus endosomal trafficking. In this study, we have used the prototype bunyavirus, Bunyamwera virus (BUNV), as a tool to understand why K.sup.+ channels are required for progression of these viruses through the endocytic network. We report three major findings: First, the production of a dual fluorescently labelled bunyavirus to visualize virus trafficking in live cells. Second, we show that BUNV traffics through endosomes containing high [K.sup.+ ] and that these K.sup.+ ions influence the infectivity of virions. Third, we show that K.sup.+ channel inhibition can alter the distribution of K.sup.+ across the endosomal system and arrest virus trafficking in endosomes. These data suggest high endosomal [K.sup.+ ] is a critical cue that is required for virus infection, and is controlled by cellular K.sup.+ channels resident within the endosome network. This highlights cellular K.sup.+ channels as druggable targets to impede virus entry, infection and disease.

Phylogenetic analyses showed that the virus responsible for a May 2024 Oropouche fever outbreak in Cuba was closely related to viruses from Brazil in 2023. Pools of Ceratopogonidae spp. biting midges and Culex quinquefasciatus mosquitoes were positive for Oropouche viral RNA. No cases were severe. Virus extension to new areas may increase case numbers and severity.

Bunyaviruses are negative sense, single-strand RNA viruses that infect a wide range of vertebrate, invertebrate and plant hosts. WHO lists three bunyavirus diseases as priority diseases requiring urgent development of medical countermeasures highlighting their high epidemic potential. While the viral large (L) protein containing the RNA-dependent RNA polymerase is a key enzyme in the viral replication cycle and therefore a suitable drug target, our knowledge on the structure and activities of this multifunctional protein has, until recently, been very limited. However, in the last few years, facilitated by the technical advances in the field of cryogenic electron microscopy, many structures of bunyavirus L proteins have been solved. These structures significantly enhance our mechanistic understanding of bunyavirus genome replication and transcription processes and highlight differences and commonalities between the L proteins of different bunyavirus families. Here, we provide a review of our current understanding of genome replication and transcription in bunyaviruses with a focus on the viral L protein. Further, we compare within bunyaviruses and with the related influenza virus polymerase complex and highlight open questions.

We demonstrated experimental acquisition and transmission of Heartland bandavirus by Haemaphysalis longicornis ticks. Virus was detected in tick salivary gland and midgut tissues. A total of 80% of mice exposed to 1 infected tick seroconverted, suggesting horizontal transmission. H. longicornis ticks can transmit the virus in the transovarial mode.

The Bunyavirales order includes at least fourteen families with diverse but related viruses, which are transmitted to vertebrate hosts by arthropod or rodent vectors. These viruses are responsible for an increasing number of outbreaks worldwide and represent a threat to public health. Infection in humans can be asymptomatic, or it may present with a range of conditions from a mild, febrile illness to severe hemorrhagic syndromes and/or neurological complications. There is a need to develop safe and effective vaccines, a process requiring better understanding of the adaptive immune responses involved during infection. This review highlights the most recent findings regarding T cell and antibody responses to the five Bunyavirales families with known human pathogens (Peribunyaviridae, Phenuiviridae, Hantaviridae, Nairoviridae, and Arenaviridae). Future studies that define and characterize mechanistic correlates of protection against Bunyavirales infections or disease will help inform the development of effective vaccines.

Sandflies are known vectors of leishmaniasis. In the Old World, sandflies are also vectors of viruses while little is known about the capacity of New World insects to transmit viruses to humans. Here, we relate the identification of RNA sequences with homology to rhabdovirus nucleocapsids (NcPs) genes, initially in the Lutzomyia longipalpis LL5 cell lineage, named NcP1.1 and NcP2. The Rhabdoviridae family never retrotranscribes its RNA genome to DNA. The sequences here described were identified in cDNA and DNA from LL-5 cells and in adult insects indicating that they are transcribed endogenous viral elements (EVEs). The presence of NcP1.1 and NcP2 in the L. longipalpis genome was confirmed in silico. In addition to showing the genomic location of NcP1.1 and NcP2, we identified another rhabdoviral insertion named NcP1.2. Analysis of small RNA molecules derived from these sequences showed that NcP1.1 and NcP1.2 present a profile consistent with elements targeted by primary piRNAs, while NcP2 was restricted to the degradation profile. The presence of NcP1.1 and NcP2 was investigated in sandfly populations from South America and the Old World. These EVEs are shared by different sandfly populations in South America while none of the Old World species studied presented the insertions.

Oropouche fever is an infectious disease caused by the Oropouche virus (OROV). The diagnosis and prediction of the clinical picture continue to be a great challenge for clinicians who manage patients with acute febrile syndrome. Several symptoms have been associated with OROV virus infection in patients with febrile syndrome; however, to date, there is no clinical prediction rule, which is a fundamental tool to help the approach of this infectious disease. To assess the performance of a prediction model based solely on signs and symptoms to diagnose Oropouche virus infection in patients with acute febrile syndrome. Validation study, which included 923 patients with acute febrile syndrome registered in the Epidemiological Surveillance database of three arbovirus endemic areas in Peru. A total of 97 patients (19%) were positive for OROV infection in the development group and 23.6% in the validation group. The area under the curve was 0.65 and the sensitivity, specificity, PPV, NPV, LR + and LR- were 78.2%, 35.1%, 27.6%, 83.6%, 1.20 and 0.62, respectively. The development of a clinical prediction model for the diagnosis of Oropouche based solely on signs and symptoms does not work well. This may be due to the fact that the symptoms are nonspecific and related to other arbovirus infections, which confuse and make it difficult to predict the diagnosis, especially in endemic areas of co-infection of these diseases. For this reason, epidemiological surveillance of OROV in various settings using laboratory tests such as PCR is important.

We used metagenomic analysis to identify Tacheng tick virus 2 infection in a patient with a history of tick bite in northwestern China. We confirmed the virus with reverse transcription-PCR, virus isolation, and genomic analysis. We detected viral RNA in 9.6% of ticks collected from the same region.