Brent Brown

Monkeypox virus (MPXV) isolation occurred in 1958, with previously non–endemic areas initially announced in 2003, with the second epidemic occurring in 2022. The third announcement occurred in 2024 was confirmed by the World Health Organisation (WHO). The second MPXV outbreak was found to be a lineage derived from clade IIb named the B1 strain; however, between 2023-2024, clade I and clade II MPXV strains are known to have sub–lineages with potential apparence of co–circulation. Historically, the now extinct variola virus (VARV) used to occur in two characterised types (minor / major), with the latter the causal agent of smallpox disease in severity. MPXV was also characterised into two clades (clade I/II), and further lineages with similar differential infection fatality rate (IFR) previously. Existing therapeutics were evaluated since 1796 and are considered further in this review as prophylactic or post–exposure prophylactics. These were investigated through homology of proteins between both MPXV and VARV since the second was eradicated. This review has three objectives. Firstly, an analysis of the epidemiology of the current MPXV outbreak, in context with other poxviruses. The second encompasses historical development of therapeutics to the above two, whilst the third spans potential future cancer therapeutics arising through investigational new drug developmental research since vaccinia virus (VACV) complete genome sequencing occurred in the 1990s.

Measles virus (Morbillivirus abbreviated as MV, but more recently MeV) is the causal agent of measles disease, thought to have existed at least 4,000 years ago, affecting predominantly infants, but also immunocompromised individuals remaining a public health issue today globally. In this review, we discuss the historical background about MeV infection to modern-day research on measles disease, current epidemiology, but also what is known about immunisation against it. We report what is known about the viral structure and the function of the viral proteins. This additionally covers the cellular structure of MeV, mechanisms, and clinical aspects of infection. Including a review of topics like cellular receptor-associated entry factors, to the immunology of MeV infection. In this review, the current knowledge of innate immune responses during infection is explained, which involves changes to chemokine and cytokine expression, finalised by the present understanding of adaptive immune responses to MeV. The genomic stability of the MeV proteins is explained and suggestive that it could be the third pathogen with eradication potential (after the variola and rinderpest viruses). Further biological and immunological clarification as to how this could occur is explained below.

Measles virus (_Morbillivirus_ abbreviated as MV, but more recently MeV) is the causal agent of Measles disease, thought to have existed at least 4000 years ago, affecting predominantly infants, but also immunocompromised individuals and others remaining a public health issue today globally. In this review, we are discussing the historical background about MeV infection to modern–day research, then delving into Measles disease and discussing what is known about immunisation against the disease. We elucidate what is known about the viral structure and the function of the viral proteins. The genomic stability of the MeV particle is suggestive that the third pathogen with the potential to be eradicated (after the Variola and Rinderpest viruses) requires further biological and immunological clarification. Here therefore covers a bow from structure and mechanism to clinical aspects of MeV infection touching topics like cellular receptor–associated factors to the immunology of MeV infection. We highlight the actual knowledge about innate immune response during MeV infection, including chemokine and cytokine expression finalised by the current understanding of adaptive immune responses to MeV.

Interferons (IFNs) were the original prototype cytokine system discovered in 20th century research. As the name interferon implies (derived from the Latin interfere-on), these proteins have immunostimulatory, primarily antiviral and antitumour properties and are synthesised and secreted between cells. Due to technological advances, processes and variable factors involved in IFN regulation can be comparatively explained by proteins expressed and genes expressed. In this review, we provide a brief introduction and background on the history of IFN research. We then provide an overview of type I IFNs, associated cells, and their receptors and outline the characteristics of type I IFN subtypes. We distinguished between the three types of IFN in the immune system of higher mammals and the associated cellular signalling mechanisms of IFNs together with IFN–inducible transmembrane proteins (IFITM) during viral infection. Additionally, we elucidated the role of IFN in viral diseases, as well as type II IFN and immunological disorders, in infections and deficiency followed by type I IFN subtypes. Errors in the IFN signal transduction and activator of transcription (STAT) protein signalling pathway during disease were analysed. This paper concludes with an examination of the role of type I/II/III interferon signalling since the discovery of the timing of interferon synthesis within immune cell pathways, examining autoantibodies, interferons and errors, and finally closing with the current understanding of interferon and immunotherapy regulation in cancer.

A) * You refer to long haulers. Do you mean long distance travellers or those with PASC or Long COVID. This is required to be defined. * You refer to IFN; please state it is type II as well. It is a cytokine used for NK and T cell measu...

Ebola virus (EBOV) is a zoonotic virus comprising of six known different species, designated within the family Filoviridae and genus Ebolavirus. The first recorded outbreak of an EBOV disease (EVD) was in Yambuku, Zaire EBOV (ZEBOV) in 1976, followed by the Sudan EBOV (SUDV) later that year. Outbreaks have been increasing throughout the 21st century, and mortality rates can reach up to 90%. Such extraordinary virulence is evidenced by a few pathogens, similar to the Marburg virus (MARV) that originated in Uganda and was first detected in Germany in 1967. The virulent nature of filovirus disease has established these related viruses as a formidable global concern. There are currently four types of Ebolaviridae species known to infect humans, with two more recently identified in other animals that are genomically different concerning cellular pathogenesis or aetiology of disease. Recent advances in understanding the pathogenesis of filovirus disease infections have been remarkable, yet the immunological response to filovirus infection remains unknown. Scientific analysis of cellular mechanisms can provide insight into virulence factors utilised by other pathogenic viruses that also cause febrile illness with occasional haemorrhagic fever in humans. In this review, a brief summary of EBOV protein structure and functional cellular effects is covered. The role of innate and adaptive immune cells known since 1976 is considered with the relevance and implications of immunological proteins measured by cluster of differentiation (CD) molecule, alongside cytokine, chemokine, and other biologically relevant pathways, and through genetic research. A thorough understanding of immunological correlates affecting host responses to EBOV will facilitate clinical and applied research knowledge, contributing to protection against potential public health threats.

* You refer to HPV. There many genotypes of HPV. Please be specific. Types 16/18 remain the dominant immunisation targets, but the others should be compared: doi: 10.1097/LGT.0000000000000494 [https://doi.org/10.1097%2FLGT.0000000000000494], DOI: 1...

Since 2019, notable global viral outbreaks have occurred necessitating further research and healthcare system investigations. Following the coronavirus disease 2019 (COVID-19) pandemic, in 2022, whilst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains evolved, monkeypox virus (MPXV) infections became more evident. MPXV is of the Orthopoxviridae genus, belonging to the family Poxviridae. Zoonotic transmission (animal-to-human transmission) may occur. The Orthopoxviridae genus includes other orthopoxviruses (OPXVs) present in animal host reservoirs that include cowpox viruses (CPXVs), vaccinia virus (VACV), and variola virus (VARV), with the latter being a causal agent of smallpox and excessive mortality. This review aims to present facts about MPXV-specific pathogenesis, epidemiology, and immunology alongside historical perspectives. MPXV was rarely reported outside Africa before April 2000. Early research since 1796 contributed towards the eradication of VARV leading to immunisation strategies. The World Health Organisation (WHO) announcement that VARV had been eradicated was confirmed in 1980. On the 23rd of July 2022, the WHO announced MPXV as a health emergency. Therefore, concern due to the propagation of MPXV causing monkeypox (mpox) disease requires clarity. Infected hosts display symptoms like extensive cellular-initiated rashes and lesions. Infection with MPXV makes it difficult to differentiate from other diseases or skin conditions. Antiviral therapeutic drugs were typically prescribed for smallpox and mpox disease; however, the molecular and immunological mechanisms with cellular changes remain of interest. Furthermore, no official authorized treatment exists for mpox disease. Some humans across the globe may be considered at risk. Historically, presenting symptoms of mpox resemble other viral diseases. Symptoms include rashes or lesions like Streptococcus, but also human herpes viruses (HHVs), including Varicella zoster virus (VZV).

The article could contextualise this further: * CFS/ME renamed in 2015 as systemic exertion intolerance disease (SEID) * In 2017 other summary reviews indicate that the causes of ME/CFS were unknown very similar to Long COVID * You mention CD57...