Herpesviruses are widespread viruses, causing severe infections in both humans and animals. Eradication of herpesviruses is extremely difficult because of their ability to establish latent and life-long infections. However, latency is only one tool that has evolved in herpesviruses to successfully infect their hosts; such viruses display a wide (and still incompletely known) panoply of genes and proteins that are able to counteract immune responses of their hosts. Envelope glycoproteins and cytokine inhibitors are two examples of such weapons. All of these factors make it difficult to develop diagnostics and vaccines, unless they are based on molecular techniques. Animal herpesviruses, because of their striking similarity to human ones, are suitable models to study the molecular biology of herpesviruses and develop strategies aimed at designing neurotropic live vectors for gene therapy as well as engineered attenuated vaccines. BHV-1 is a neurotropic herpesvirus causing infectious rhinotracheitis (IBR) in cattle. It is a major plague in zootechnics and commercial trade, because of its ability to spread through asymptomatic carrier animals, frozen semen, and embryos. Such portals of infections are also important for human herpesviruses, which mainly cause systemic, eye, and genital tract infections, leading even to the development of cancer. This review covers both the genetics and molecular biology of BHV-1 and its related herpesviruses. Epidemiology and diagnostic approaches to herpesvirus infections are presented. The role of herpesviruses in gene therapy and a broad introduction to classic and engineered vaccines against herpesviruses are also provided.

Environmental transmission of Chlamydia abortus as a result of enzootic disease or disease outbreaks and the threats posed by this pathogen has been previously reported, however a state-of-the-science review of these reports and the identification of future research priorities in this area is still lacking. This study provides an overview of the current knowledge of host–pathogen–environment interactions, addressing public health risks and identifying critical questions and research gaps. We performed a systematic PubMed and Web of Science search for publications related to Chlamydia abortus in the past four decades, and we reviewed and combined the evidence critically discussing and commenting the results. A total of 182 studies, 5 chapters of specific books and the “OIE terrestrial manual” were included in this review. There were substantial variations between the studies in topic addressed and experimental design. Overall, the literature largely supports the crucial role played by environmental exposure on the acquisition of zoonotic disease caused by Chlamydia abortus. We also identify the paucity of information related to interspecies transmission and pathogen adaptation in relation to environmental dissemination and zoonotic risk. This analysis further highlights the need for additional research given that environmental transmission represents a serious risk not only to susceptible patients (pregnant women and immunocompromised individuals), but also for other species including wildlife.

Mutations in the intracellular juxtamembrane domain of the c-kit gene in 32 dogs with different grades of histologically confirmed mastocytoma were studied. Transcript RNAs extracted from neoplastic tissue surgically collected from dogs of different breeds and from a negative control were reverse transcribed into complementary DNA and amplified by polymerase chain reaction. The region corresponding to the c-kit juxtamembrane domain was sequenced and compared with GenBank sequences. Two different types of mutations were identified within exon 11: a previously underscribed single-nucleotide substitution and a 6-bp deletion. The c-kit juxtamembrane domain sequences of all dogs were grouped in 3 clusters. No mutations were detected in tissues constitutively expressing c-kit (cerebellum and spleen), obtained from dogs not affected by mastocytoma (controls). All the substitutions were found in dogs bearing grade I or II mast cell tumors; the deletion was detected in 1 dog with grade II mastocytoma.