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Origin of HIV
Published in Omar Bagasra, Donald Gene Pace, A Guide to AIDS, 2017
Omar Bagasra, Donald Gene Pace
As human beings, we are exposed to numerous microbes that originated from chimps or other primates. For example, monkeys transmit yellow fever, falciparum malaria, Kyasanur Forest disease, tanapox, and Mayaro. These viruses then rely on mosquitoes, ticks, and biting flies to transmit disease from monkeys to humans. Simian virus 40 (SV-40) is present in macaque monkeys, and most people were exposed to it through vaccines that contained monkey tissue in the early days of Albert Sabin’s live polio vaccination [1,2]. None of these diseases are as fatal as HIV. If untreated, HIV is almost 100% fatal. Why? How can a disease that is essentially innocuous to chimps be so fatal to its human hosts? Let us stress here that the notion that HIV invaded human hosts because they ate chimp meat and hunted them is so obviously ridiculous and contrived that it defies the common sense [3,4–5]. Man has been hunting monkeys and chimps for eons of time. Why, then, after so many years, did acquired immune deficiency syndrome (AIDS) arrived precisely at the time when the oral polio vaccine was given to more than a million people in Congo in the mid- to late-1950s? There is no physical evidence that HIV existed before this particular time period. Physical evidence for the earliest HIV sample is from 1959 (published by David Ho’s team from Aaron Diamond Institute of New York [6]). In Section 6.3, we will discuss and provide scientific evidence for how HIV-1 emerged and came into humans, why it is so deadly for us but not to chimps, and why it is able to evade our highly evolved immune defense systems? Investigation into the origins of HIV-1 is critical in development of a cure for HIV-1. We do not intent to deride or blame anyone. Our goal is to honestly present the information as we see it, which we hope will lead to finding the cure for HIV-1/AIDS and to the development of a vaccine and effective therapeutics. No vaccine or cure for a deadly disease has ever come about without knowing the origin or cause of the disease (with the rare exception of smallpox).
Mpox: epidemiology, clinical manifestations and recent developments in treatment and prevention
Published in Expert Review of Anti-infective Therapy, 2023
Nikil Selvaraj, Shreya Shyam, Puvin Dhurairaj, Kaviarasan Thiruselvan, Akil Thiruselvan, Yochana Kancherla, Pritika Kandamaran
Double-stranded deoxyribonucleic acid viruses belonging to the Poxviridae family infect a variety of species, including birds, reptiles, insects, and mammals [5]. The family is divided into two subfamilies: Entomopoxvirinae and Chordopoxvirinae, which together contain 52 species and 18 genera (with 4 genera and 30 species). The Chordopoxvirinae subfamily of the Poxviridae family, which includes the genus Orthopoxvirus, is where Mpox originates [5]. Variola (smallpox), cowpox, Mpox, vaccinia, camelpox, alaskapox, yaba monkey tumor virus, tanapox virus, orf virus, pseudocowpox virus, bovine papular stomatitis virus, buffalopox, and molluscum contagiosum are some of the poxvirus species that have been linked to human diseases [5]. Variola and molluscum contagiosum viruses are reservoir hosts in humans (Figure 1). As the Mpox virus (MPXV) can infect a broad variety of creatures, it circulates in wild animals while sporadically infecting humans through spillover episodes [6]. It is important to remember that infection with any one virus of a genus has shown to offer some protection against infections with any other viruses within the same genus [5].
Exploitation of receptor tyrosine kinases by viral-encoded growth factors
Published in Growth Factors, 2018
The first EGF-like ligand encoded by a virus was identified in the genome of Vaccinia virus (VACV), a member of the Orthopoxviruses in the Poxvirus family (Twardzik et al., 1985). Variants of the EGF-like protein were then recognized as conserved sequences in other orthopoxvirus, such as Variola virus (VARV) (Kim et al., 2004), Ectromelia virus (ECTV) (Chen et al., 2003), Monkeypox virus (MPXV) (Shchelkunov et al., 2002), and Cowpox virus (CPXV) (da Fonseca et al., 1999). Following this discovery, EGF-like ligands were located in the genomes of Leporipoxviruses, including Myxoma virus (MYXV) (Upton et al., 1987) and Shope Fibroma virus (SFV) (Chang et al., 1990). Sequencing of Fowlpox virus (FWPV), a member of the Avipoxviruses, also showed the presence of EGF-like protein sequences (Afonso et al., 2000). The FWPV EGF-like protein is highly conserved amongst the seven avipoxvirus genomes currently available for comparison, including pigeon pox virus (PGPV) and canarypox (CNPV) (Carulei et al., 2017). More recently an EGF-like ligand expressed by Tanapox virus (TANV), a member of the Yatapoxviruses, was identified. Open reading frames with similarity to the TANV EGF-like gene have now been identified in another Yatapoxvirus, Yaba-like disease virus (YLDV) (Lee et al., 2001), and in Capripoxviruses, including Goatpox virus (GTPV), Lumpy skin disease virus (LSDV), and Sheeppox virus (SPPV) (Jeng et al., 2013). EGF homologs have not been reported in any virus outside of the Poxvirus family.
Virotherapy: Current Trends and Future Prospects for Treatment of Colon and Rectal Malignancies
Published in Cancer Investigation, 2019
Chin Liang Lee, Sanggeetha Veeramani, Aidin Molouki, Swee Hua Erin Lim, Warren Thomas, Suet Lin Chia, Khatijah Yusoff
Tanapoxvirus causes a febrile disease in humans and was first identified from outbreaks in central Africa in the 1950s and 1960s. Like other poxviruses tanapox can be attenuated through the deletion of genes essential for virus replication. A tanapoxvirus deficient in TK and a TNF binding protein was effective in causing tumour regression in a nude mouse CRC xenograft model, the effect was enhanced by expression of the bacterial flagellin fliC gene [107]. The fliC protein is effective in stimulating an innate immune response, demonstrating the importance of innate immunity in poxvirus-induced cytotoxicity.