Papovaviridae Group 7 PDF
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Casauay, Carlo Jay,Dugay, Eunice,Lemi, Katrina Alyssa,Mangusad, Aprille,Siruno, Dan Karlo
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This document provides an overview of Papovaviridae, focusing on the morphology, taxonomy, and differences between papillomaviruses and polyomaviruses. The document also includes details on various species and their diseases. It appears to be a study guide or notes for a biology course.
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Group 7: Casauay, Carlo Jay Dugay, Eunice Lemi, Katrina Alyssa Mangusad, Aprille Siruno, Dan Karlo PAPOVAVIRIDAE I. Introduction Papovaviridae is a former family of a double stranded DNA viruses that include the polyomaviruses and the pa...
Group 7: Casauay, Carlo Jay Dugay, Eunice Lemi, Katrina Alyssa Mangusad, Aprille Siruno, Dan Karlo PAPOVAVIRIDAE I. Introduction Papovaviridae is a former family of a double stranded DNA viruses that include the polyomaviruses and the papillomaviruses before they were placed in their own families. A. Papillomaviruses - Ubiquitous but highly host-species specific. - Majority of papillomavirus infections do not result in obvious lesions. However, infection by some papillomavirus types can cause visible papillomas on the skin or mucosal membranes.P - Papillomavirus-induced papillomas are called “warts” B. Polyomaviruses - Recognized as a separate virus family since 2000. - Like papillomaviruses, polyomaviruses are ubiquitous and the vast majority of infections occur without clinical consequence (most infections caused by these viruses do not lead to noticeable symptoms or health issues. i.e., most people carry these viruses without experiencing any adverse effects) - Highly host-species specific. Table 1: Similarities and differences between Papillomaviruses and Polyomaviruses Papillomaviruses vs Polyomaviruses Similarities Differences Genome organization Taxonomy Virion structure Biology Mechanisms of replication and cell cycle regulation Biological features: Mechanisms of tumor induction Ability to cause persistent infections of their hosts. II. Morphology A. Papillomaviruses Shape: Icosahedral and non-enveloped Size: 52-5 nm in diameter Composition: 80% protein and 20% DNA Genome: circular dsDNA with about 8000 bases-pairs Capsid: Made of 72 pentamers of capsid viral protein B. Polyomaviruses Shape: Icosahedral and non-enveloped Size: 40.5-44 nm in diameter Composition: 88% protein and 12% DNA Genome: Circular, dsDNA with about 5000 base pairs Capsid: Made of 72 pentamers of capsid viral protein 1 (VP1) Figure 1: Representation of Human Papillomavirus capsid structure. L1 – major capsid protein. Figure 2: Representation of Polyomavirus capsid structure. VP1 – major capsid protein; VP2 – minor capsid protein; VP3 – minor capsid protein. Terms: L1 – major capsid protein of papillomaviruses which plays a role in capsid structure and formation, viral entry, DNA encapsulation, immunogenicity (i.e., it can elicit strong immune response). L2 – minor capsid protein of papillomaviruses which assist in stabilizing the viral genome and facilitating its transport into host cells. VP1 – major capsid protein of polyomaviruses which assembles with other proteins (like VP2 and VP3) to form protomers, which then combine to create the complete virion. It is also involved in binding to specific receptors on host cells. Just like L1, it is highly immunogenic which has been targeted in vaccine development. VP2 and VP3 – significantly smaller than VP1, has a role in viral entry into host cells and may assist in packaging the viral genome into the capsid. III. Taxonomy A. Papillomavirus - Papillomaviridae are currently divided into 39 genera that are named using the Greek alphabet. The papillomaviruses included within each genus typically share their host- species specificity and biological properties, including the disease they cause. Within genera, the papillomaviruses that show the greatest similarity are then grouped into numerically-named species. Kingdom: Shotokuvirae Phylum: Cassaviricota Class: Papovaviricetes Order: Zurhausenvirales Family: Papillomaviridaae Genus: o Alphapapillomavirus o Betapapillomavirus o Gammapapillomavirus o Deltapapillomavirus o Epsilonpapillomavirus o Zetapapillomavirus o Etapapillomavirus o Thetapapillomavirus o Iotapapillomavirus o Kappapapillomavirus o Lambdapapillomavirus o Mupapillomavirus o Nupapillomavirus o Xipapillomavirus o Omikronpapillomavirus o Pipapillomavirus o Rhopapillomavirus o Sigmapapillomavirus o Taupapillomavirus o Upsilonpapillomavirus o Phipapillomavirus o Psipapillomavirus o Omegapapillomavirus B. Polyomavirus Kingdom: Shotokuvirae Phylum: Coassaviricota Class: Papovaricetes Order: Sepolyvirales Family: Polyomaviridae Genus: o Alphapolyomavirus o Betapolyomavirus o Deltapolyomavirus o Epsilonpolyomavirus o Etapolyomavirus o Gammapolyomavirus o Thetapolyomavirus o Zetapolyomavirus IV. Pathology A. Infection mechanism - Papillomaviruses typically infects the basal epithelial cells through microtrauma or abrasions in the skin or mucosal surfaces. Once inside, it can establish a productive infection, leading to the formation of papillomas (warts) that may regress or progress to malignancy over time. B. Viral replication - Papillomaviruses replicate its DNA in the nucleus of infected cells, utilizing cellular machinery. The replication is closely tied to the differentiation of keratinocytes, with viral gene expression being regulated by the host cell’s state. V. Specie Specific Diseases A. Papillomaviruses 1. Cattle Disease Associated Papillomavirus Fibropapilloma and squamous papilloma BPV- 1 to BPV-13 (BPV – Bos taurus of the skin, teat, genitals, and rostral oral papilloma virus) cavity Squamous papilloma of the upper BPV-4 alimentary tract Bladder neoplasia BPV-2 Upper alimentary tract squamous cell BPV-4 carcinoma a. Distribution o Global (more common in housed cattle than on cattle on pasture) b. Transmission o Direct contact with contaminated surfaces (e.g., milking equipment, halters, and grooming tools) o Possible sexual transmission (genital papillomas) c. Pathogenesis o Fibropapillomas and squamous papillomas; BPV-4 may cause alimentary neoplasia with bracken fern exposure d. Diagnosis o Clinical examination o Skin biopsy e. Prevention/Treatment o Vaccines o Surgical removal for interfering lesions o Spontaneous regression is common 2. Horse Disease Associated Papillomavirus Cutaneous squamous papilloma EcPV-1 (EcPV – Equus caballus papillomavirus) Penile and preputial papilloma and EcPV-2 squamous cell carcinoma Aural plaques EcPV- 3, -4, -5, -6. Sarcoid BPV-1, -2, -13 a. Distribution o Global (more common in young horses) b. Transmission o Fomites o Direct contact (sarcoid linked to BPV) c. Pathogenesis o Papillomas often regress; o Aural plaques and sarcoid persist, with sarcoids having high recurrence. d. Diagnosis o Clinical examination of lesions o Biopsy for confirmation of squamous cell carcinoma e. Prevention/Treatment o Surgical excision for cutaneous papillomas 3. Dog Disease Associated Papillomavirus Oral papillomas CPV-1 (CPV – Canis domesticus papillomavirus) Cutaneous papilloma CPV-2, -6 Cutaneous pigmented plaque CPV -3, -4, -7, -8, -9, -10, -11, -14, -15, -16 a. Distribution o Global (more common in younger dogs) b. Transmission o Fomites o Direct contact c. Pathogenesis o Oral papillomas regress in weeks o Pigmented plaques become squamous cell carcinoma d. Diagnosis o Clinical examination o Biopsy or histopathology for persistent or suspicious lesions e. Prevention/Treatment o Spontaneous regression (most papillomas and plaques) o Surgical intervention for persistent or problematic lesions 4. Cat Disease Associated Papillomavirus Cutaneous plaque FcaPV-1, -2, -3 (FcaPV – Felis catus Bowenoid in situ carcinoma papillomavirus) Cutaneous squamous cell carcinoma Sarcoid BPV-14 a. Distribution o Cutaneous plaque/Bowenoid: US, Australia, European countries, and Canada o Cutaneous cell carcinoma: US, Australia, New Zealand, and Southern Europe o Feline sarcoid: US, UL, Australia, European countries, and South Africa b. Transmission o Direct contact o Feline sarcoid: Direct contact, Fomites, Environmental exposure, wound infections c. Pathogenesis o Cutaneous plaque: Raised, scaly plaques, usually asymptomatic o Bowenoid: Red, scaly patches, often asymptomatic but may itch o Cutaneous scc: Firm nodules or ulcers that may be painful or bleed o Feline sarcoid: Skin growths: the most prominent sign is the presence of raised, wart-like growths on the skin d. Diagnosis o Clinical examination o Biopsy o Dermatoscopy o Sarcoid: Cytology e. Prevention/Treatment o Sun protection o Surgical removal o Cryotherapy o Laser therapy o Sarcoid: Vaccination 5. Rabbit Disease Associated Papillomavirus Oral papilloma OcPV-1 (OcPV – Oryctolagus cuniculus papillomavirus) a. Distribution o US, Canada, European countries, Australia, New Zealand b. Transmission o Fomites o Direct contact o Mucosal exposure c. Pathogenesis o Visible growths of lesions o Difficulty eating o Drooling o Bad breath o Swelling o Weight loss d. Diagnosis o Clinical examination o Biopsy o Histopathology e. Prevention/Treatment o Quarantine o Good hygiene 6. Psittacines (Parrots) Disease Associated Papillomavirus Cloacal papillomatosis PsPV a. Distribution o Worldwide, especially New World parrots o South/Central America b. Transmission o Direct contact especially during breeding c. Pathogenesis o Cloacal/Oral papilloma o Cloacal prolapse o Bloody droppings d. Diagnosis o Visual inspection o Biopsy confirmation e. Prevention/Treatment o Surgical removal B. Polyomaviruses 1. Geese Disease Associated Polyomavirus Goose Hemorrhagic Nephritis and Goose Hemorrhagic Polyomavirus Enteritis (GHNE) a. Distribution o Mostly Europe and Asia b. Transmission o Horizontal (Fecal-Oral) c. Pathogenesis o Sudden death o Hemorrhages o Lethargy o Diarrhea d. Diagnosis o Histopathology o PCR o Virus isolation e. Prevention/Treatment o No specific antiviral therapy o Supportive care 2. Budgerigars (and other psittacines) Disease Associated Polyomavirus Budgerigar Fledgling Disease (BFD) Avian polyomavirus a. Distribution o Worldwide b. Transmission o Horizontal: Direct contact, feather dust o Vertical: Eggs c. Pathogenesis o Sudden death o Abdominal distension o Feather abnormalities o Immune suppression d. Diagnosis o PCR o Histopathology (inclusion bodies) o Serology e. Prevention/Treatment o Supportive care o Vaccination 3. Laboratory Animals (Monkeys, mice, rats, hamsters, and rabbits) Disease Associated Polyomavirus Kidney disease Murine polyomavirus (MPyV) Tumors Acute infection Progressive Multifocal Simian virus 40 (SV40) Leukoencophalopathy Lymphoma SV40 a. Distribution o North America, Europe, Asia (SV40) b. Transmission o MPyV: Direct contact, Fomites, Aerosolized particles o SV40: Aerosol transmission, fecal-oral route, contaminated equipment, vertical transmission o SV40 (lymphoma): same above except vertical transmission c. Pathogenesis o MPyV: ▪ Weight loss ▪ Lethargy ▪ Visible masses (particularly in abdomen and around kidney) o SV40 ▪ Weakness (especially in limbs) ▪ Ataxia ▪ Visual impairments ▪ Tremors o SV40 (Lymphoma) ▪ Swollen lymph nodes ▪ Weight loss ▪ Letahrgy ▪ Abdominal distention d. Diagnosis o Clinical observation o PCR testing o Serological Tests o Histopathology e. Prevention/Treatment o MPyV: ▪ Supportive care ▪ Culling ▪ Environment management o SV40 ▪ Address underlying conditions ▪ Discontinue immunosuppressive therapy ▪ Supportive care ▪ Experimental therapies (therapies aimed to reactivate immune responses o SV40 (Lymphoma) ▪ Vaccination (HPV, Hepatitis) ▪ Chemotherapy ▪ Radiation therapy ▪ Immunotherapy ▪ Supportive care References: Boothpur, R., & Brennan, D. C. (2010). Human polyoma viruses and disease with emphasis on clinical BK and JC. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology, 47(4), 306–312. https://doi.org/10.1016/j.jcv.2009.12.006 IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Human Papillomaviruses. Lyon (FR): International Agency for Research on Cancer; 2007. (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 90.) From: https://www.ncbi.nlm.nih.gov/books/NBK321760/ MacLachlan, N.J., & Dubovi, E. (2017). Fenner’s Veterinary Virology: Fifth Edition. Academic Press Elsevier. ISBN: 978-0-12-800946-8 Fernandes, Jos & Fernandes, Thales. (2012). Human Papillomavirus: Biology and Pathogenesis. 10.5772/27154. From: https://www.researchgate.net/publication/221922588_Human_Papillomavirus_Biology_and_ Pathogenesis/citation/download Bennett, S.M. (2014). Intracellular Trafficking of BK Polyomavirus: From the ER to the Nucleus. Cellular and Molecular Biology in University of Michigan. From: https://deepblue.lib.umich.edu/bitstream/handle/2027.42/107123/shaunamb_1.pdf%3Bjsessio nid%3DAC4796E444740BA77A6C2CA83CD0D5E6?sequence%3D1 https://ictv.global/taxonomy