Recommended
Recommended
More Related Content
What's hot
What's hot (20)
Similar to virus in periodontics
Similar to virus in periodontics (20)
Recently uploaded
Recently uploaded (20)
virus in periodontics
- 1. VIRUS D R FAV E E N N A S U K U M A R A N P G - I I Y E A R ROLE OF IN PERIODONTAL DISEASE
- 2. ⢠Introduction ⢠General Virology ⢠Morphology ⢠Classification ⢠Cultivation ⢠Human Viruses & Diseases ⢠Viruses in Periodontal Disease ⢠Summary & Conclusion
- 4. Smallest living unit Infective agent Multiply inside living cells VIRUS
- 5. Based on 1999 International Workshop for the Classification Viral diseases of the periodontium placed under non-plaque induced gingival lesions, and they include herpetic gingivostomatitis, varicella zoster and others
- 8. DNA Herpes simplex virus Varicella-zoster virus Epstein-Barr virus CytomegalovirusHuman herpes virus 6 Pox viruses Papillomavirus Hepatitis B virus Influenza virus, Paramyxoviruses, Mumps Measles, Rubella, Human immunodeficiencyRabies Rotavirus Picornaviruses, Rhinovirus Polio virus RNA
- 10. NON ENVELOPED ENVELOPED Components Proteins Lipids , proteins , glycoproteins Properties â˘Environmentally stable â˘Resistant to stresses such as temperature , acid , detergents , drying â˘Environmentally labile â˘Disrupted by acid , detergents drying, heat Released by cell lysis Released by budding or cell lysis Transmission Fomites , hand to hand , dust Large droplets , secretions , blood Dry out but retain infectivity Must stay wet Immunity Controlled mainly by antibodies Antibodies and cell mediated immunity
- 11. Inoculation into animals Embryonated Eggs Organ culture Explant culture Cell culture CULTIVATION Tissue Culture
- 16. VIRUSES IN PERIODONTAL DISEASES
- 18. contracted in childhood Infected -saliva cause lesions in the oral cavity during primary infection â˘After primary infection the virus became latent
- 19. Physical injury Trauma Sunlight Surgery Cold Fever Immune suppression Upper respiratory tract infection Wind Emotional stress Physiological event menstruation Latent virus can be triggered by
- 20. Alpha Herpes virus Beta Herpes virus Gamma Herpes virus HERPES VIRUS
- 21. HSV 1 ⢠That sheds in saliva Transmitted ⢠Directly ⢠Indirectly Cause ⢠Oral facial infections and encephalitis
- 22. HSV2-transmitted sexually and causes genital infection Other ways of transmission- auto inoculation by fingers to eye or genital tract Infected mother to neonates
- 24. Herpes virus Periodontopa thic potential Direct cytopathi c effect Hamper the cells in host defence Increased level- periodont al pathogen Alters the inflamma tory pathway Suppressin g release MHC Class I
- 26. Pathogenesis HSV associated periodontal disease ⢠Direct cytopathic effect on fibroblast, keratinocytes etc. impairs the cell involved in host defense ⢠It promotes subgingival attachment and colonization of periodontal pathogenic bacteria ⢠That cause altered inflammatory mediators and cytokine pathway ⢠Increase in IL 1B and TNF alpha ⢠Tissue injury as result of immunologically response to virally infected cells
- 27. Maintenance of fluid & food intake Antipyretic & Analgesics Topical antiseptics to prevent bacterial superinfections Acyclovir -500/1000mg per day
- 32. Herpes zoster results from reactivation of virus that remain latent in sensory ganglia Apparition of lesions -severe pain and paresthesia Alveolar bone necrosis
- 33. Vaccination for varicella - part of the routine vaccination Children - 2 doses : at age 12 to 15 months at age 4 to 6 years Teenagers and Adults who have not had the vaccine or the disease. Two doses 4 to 8 weeks apart.
- 35. EpsteinâBarr virus Transmitted Oral secretions Blood
- 38. EBV -associated to other diseases - cancers and auto- immune diseases (Thorley-Lawson and Gross, 2004). OHL is the main lesion associated to EBV Most often a relatively advanced stage of HIV infection
- 40. 10% of infants are infected by the age of 6 months ⢠Mother-placenta during delivery ⢠Breast feeding Transmission
- 45. HEPATITIS VIRUS
- 46. HEPATITIS A VIRUS Non enveloped Single stranded Rarely fatal and does not lead to chronic liver disease
- 47. Transmission Feco oral route Hematogenous spread
- 49. HEPATITIS B VIRUS Most important type of viral hepatitis Recovery 1- 2 months chronic subclinical infection Incubation period about 1-6 months HBV more infectious than HIV
- 50. Child-to-child Contaminated needles Sexual contacts Healthcare worker Blood transfusion ⢠6% of people infected over the age of 5 become chronically infected Perinatal ⢠90% of infected infants become chronically infected PERINATAL TRANSMISSION TRANSMISSION OF HBV CDC. Available at: http://www.cdc.gov/hepatitis. Accessed December 2006. Lee WM. N Engl J Med. 1997;337:1733-1745. Lavanchy D. J Viral Hepat. 2004;11:97-107. HostMother Infant Recipient HORIZONTAL TRANSMISSION
- 52. symptoms
- 54. Detection of viral markers-HBsAg,HBeAg,HBcAg Viral DNA Polymerase Polymerase Chain Reaction (PCR)
- 55. Passive immunization ( HBIG) IM 300- 500 iu Child born to carrier mothers 0.5ml of HBIG immediately after birth Complete course first injection being given within 12 hrs of birth. Active immunization Non glycosylated HBsAg -IM 3 dosesâŚ0,1,6 months. . ..
- 56. . . Twinrix, which combines both the Hepatitis A and Hepatitis B vaccines and it includes only 3 injections- protection against both Hepatitis A & B vaccines are very powerful & long term protection. Hepatitis B vaccines 3inj & Hepatitis A vaccines 2 injections
- 57. HEPATITIS C VIRUS âNON-A, NON-Bâ HEPATITIS
- 58. SOURCES OF INFECTION Sexual 15% Injecting drug use 60% Transfusion 10% (before screening)
- 59. FACTORS PROMOTING PROGRESSION OR SEVERITY Other co- infections (e.g., HBV) Male gender HIV co- infection Age > 40 years at time of infection Increased alcohol intake
- 62. Blood testing ⢠Hepatitis C antibody test ⢠Hepatitis C PCR test to find virus in blood Serologic tests to HCV antibodies: ⢠enzyme immunoassay (EIA). ⢠- recombinant immunoblot assay (RIBA) ⢠Target amplification technique to detect HCV RNA (molecular assay) Liver function tests Serum ALT Liver Histology Liver biopsy
- 63. Can we prevent hepatitis c infection ??????
- 66. T R A N S M I T T E D HEPATITIS G VIRUS HGV RNA found in patient with ⢠Acute, Chronic and Fulminant hepatitis ⢠Hemophiliacs ⢠Multiple transfusion ⢠Blood donors
- 68. PERIODONTAL DISEASES ASSOCIATED WITH HIV
- 69. PATHOGENESIS
- 70. ⢠Improved health status ⢠Viral plasma bioloads below detectable level ⢠Virus never irradicated,CD4 cells got sequestered Long term use Impaired immune function Immune system failure Malignancy-disseminated infections Adverse drug reaction
- 73. CATEGORY A CATEGORY B CATEGORY C Patients with acute symptoms or asymptomatic diseases & individuals Persistent Generalised Lymhadenopathy, malaise, fatigue and low grade fever. (CD4 count >500) Symptomatic conditions like oropharyngeal or vulvovaginal candidiasis, herpes zoster, oral hairy leukoplakia, fever, diarrhea and weight loss (CD4 count 200-499) Patients with AIDS as manifested by life threatening conditions . (CD4 count< 200)
- 74. Nucleoside Reverse Transcriptase Inhibitor (NRTI) Lamivudine (Epivir) Zidovudine (Retrovir) Nonnucleoside Reverse Transcriptase Inhibitor (NNRTI) Etravirine (Intelence) Nevirapine (Viramune,) Atazanavir (Reyataz) Ritonavir (Norvir) Protease Inhibitor (PI) Fusion Inhibitor (FI) Enfuvirtide (Fuzeon, T20) Entry Inhibitor-CCR5 Co-receptor Antagonist ANTIRETROVIRAL DRUGS
- 75. SEVERE WEIGHT LOSS PERSISTENT HEADACHE HIGH FEVER WHITE PATCHES ON TONGUE HEAVY NIGHT SWEATS LOSS OF APPETITE MEMORY LOSS CHRONIC DIARRHEA FATIGUE & MUSCLE WEAKNESS SWELLING LYMPH NODES SYMPTOMS OF HIV INFECTION
- 76. MALIGNANT LYMPHOMA TOXOPLASMOSIS ENCEPHALITIS PNEUMOCYTOSIS CARNII PNEUMONIA CYTOLOMEGALOVIRUS RENTITIS HERPES SIMPLEX VIRUS CRYPTOCOCCAL MENINGITIS ORAL CANDIDIASIS KAPOSIâS SARCOMA CRYPTOSPONDIOSIS AIDS RELATED ILLNESS & OPPORTUNISTIC INFECTIONS PULMONARY TUBERCULOSIS CANDIDA OESOPHAGITIS
- 80. NECROTIZING ULCERATIVE STOMATITIS (NUS) NUS may be severely destructive and acutely painful and may affect significant areas of oral soft tissue and underlying bone. Separately or as an extension of NUP and is often associated with severe suppression of CD4 cells and elevated viral load.
- 81. DRYNESS OF THE MOUTH (XEROSTOMIA)
- 85. Pathophysiologic relationship between mammalian viruses and PD disease has the potential to extend our insight into mechanism PD tissue breakdown Based on the current information it seems reasonable to add PD disease to list of infectious disease that have HCMV , EBV and other viruses as contributory causes.
- 86. 1. Oral viral infections of adults. JORGEN SLOTS. Periodontology 2000, Vol. 49, 2009, 60â86 2. International Journal of Contemporary Dental and Medical -Viruses in periodontics Bharati Kolliyavar1 Anand Patil, Srinath L. Takur 3. Journal of dentistry,oral disorders and thearpy-Virus Associated Periodontal Diseases: Futuristic Implications Amit Parashar1, Sheetal Sanikop1, Abhishek Zingade1, Shashi Parashar and Shikha Gupta 4. Viruses in periodontal disease â a review I Cappuyns, P Gugerli, A Mombelli
- 87. 5. Human viruses in periodontitis. JORGEN SLOTS. Periodontology 2000, Vol. 53, 2010, 89â110 6. Herpesviruses in periodontal diseases. JORGEN SLOTS. Periodontology 2000, Vol. 38, 2005, 33â62 7. Periodontal disease in HIVâ AIDS. Periodontology 2000, Vol. 60, 2012, 78â 97 8. Bacterial and viral pathogens in saliva: disease relationship and infectious risk. Periodontology 2000, Vol. 55, 2011, 48â69. 9. Ananthanarayan panikerâs Textbook of Microbiology 10. C.P.Baveja-Textbook of Microbiology for dental students 11. Clinical Periodontology; Carranza X edition
- 88. THANK YOU!!!!
Editor's Notes
- Periodontal diseases are multifactorial in nature and many etiological agents are suggested to play a role in their etiopathogenesis. specific bacteria were considered the major pathogens for the disease. The current evidence strongly suggests the presence of many strains of viruses in the periodontal environment.
- ,its too small to be seen by light microscopy is an infective agent that typically consists of a nucleic acid molecule in a protein coat it cn multiply only within the living cells of a host.
- The most recent classification is based on the 1999 International Workshop for the Classification of the Periodontal Diseases organized by the American Academy of Periodontology. Here were viral diseases of the periodontium placed under nonâplaque induced gingival lesions, and they include herpetic gingivostomatitis, varicella zoster and others
- Baltimore clasifictn developed by davidn blatimore âvirus classification system tht grps viruses in to families depending on their type of genomes DNA RNA single stranded double stranded enveloped non enveloped and their method of replication
- Virus consist of nucleic acid surrounded by protein coat-capsid,function of tis capsid to protect he nucleic acid frpm inactivation by nucleases or from other deleterious agents Caspids are formed by large number of caspomers which forms the morphological unit,one of th majrvrole of capsid is to introduce viral genome into host cells Virus may be enveloped or non enveloped..envlopd or outr covring us derived from host cell membrane it s lipo protein in nature Protein subunits are seen on envlop as spikes-peplomers
- FOMITES-OBESCT WHICH LIKELY CARRY INFECTION SUCH AS CLOTHES UTENSILS FURNITURE
- Inoculation into animals- Reed & Co workers 1900âŚ- Landsteiner et al 1909⌠/ Theiler 1903⌠Embryonated Eggs- Goodpasture 1931âŚ- Allantoic Cavity⌠Tissue Culture- Steinheardt 1913âŚ- Robbins et al 1949
- It has about six steps adsorption penretration replication assembly maturation release
- It s doubl stranded DNA virus herpes simplex virus 1 and 2 also known as human herpesvirus 1 and 2 are two members of theherpesvirus family,
- Virus get reactivated in variousconditions The main cause of reactivation is immune loss, and these infections may cause severe diseases in HIV infected Most dna virus involved in periodntl infections thru contct wth saliva blood or gentisal secretions,,this remain latent in dorsal root of trigeminal gsnglion activated by emotionasl stress infection drugs fever etc
- ,,,,,,, and
- Alpha-HSV-1 and HSV-2, varicella zoster virus (VZV). subfamily has a fast growing pattern, lyse-infected cells and remain latent in sensory nerve ganglia. They induce vesiculous lesions in skin or mucosa. Beta and cmv,human herpes v 6nd 7 replication is slow nd produces lrge, often multinucleated cells genome remains latent in lymphoreticular tissue, secretory gland ,kidneys and other tissues. Gamma-hv EpsteinâBarr virus (EBV) and human herpes virus 8 (HHV-8). They infect lymphoid cells (lymphocytes B and T) but they can also be cytocidal for epithelial cells and fibroblast Latency of this subfamily frequently occurs in lymphoid tissues. EBV is responsible for infectious mononucleosis and HHV-8 may be implicated in Kaposiâs sarcoma
- Infections HSV-1 and HSV-2 are worldwide spread and usually aďŹect skin and mucosa Herpes simplex viruses are transmitted by close person-to-person contact by mucosal secretion or lesions.
- â most common gingival disease of viral origin⌠gingivitis, vesicles that leave ulcerations, cervical lymphadenopathy, fever increased salivation and bad breath. Rarely, chills, myalgia, dysphagia, or hearing loss may occur
- the primary HSV infection, virions travel from the initial site of infection on the skin or mucosa to the sensory dorsal root ganglion, where latency is established. When the dormant virus in the ganglion is activated, it begins to multiply again and moves down the trigeminal nerve usually to the site of initial inoculation and infect the epithelial cells causing a recurrent infection.This is considered as ganglion trigger theory the skin trigger theory proposed by Hill and Blyth, holds that virus is continuously shed from neuronal endings and lesions develop when the susceptibility of the skin is sufficiently permissive for the development of a clinically apparent infection
- 1 on ďŹbroblast, keratinocytes, n inďŹammatory cells -neutrophils,lymphocytes macrophages, and possibly Since the above cells are key constituents of inďŹamed peridntl tisue, herpes will bring abt cellular chnges which may aďŹect tissue turnover and repair 2 thereby prejudice to microbial super infection. HCMV ad EBV can infect and/or alter functions of monocytes, macrophages and lymphocyte herpes virus infection may bring about allocation and growth of periodontal bacteria And response of cytokines. In periodontitis,HCMV infection can upregulate IL-1β nd TNF-Îą gene expression of monocytes and macrophages. Increased production of the proinďŹ ammatory cytokines IL-1β and TNF-Îą by macrophages nd monocyts increased chance of development of periodontal disease 5 HCMV and HSV can bring about the inhibition of cell- mediated immunity by suppressing the release of MHC Class I molecules, thereby interfering with T-lymphocyte recognition -resulting in decrease in circulating CD4 cells and increase in CD8 suppressor cells, which leads to overall impairment of cell-mediated immunity
- Bacteria in the dental biofilm induce ingivitis wch permits latent herps embede n b cells macrophg tce;; to infiltrate in to periodontum.reactivation of hsv occur due to
- Varicella zoster virus (VZV) its double stranded dna virus .is one of eight herpesviruses known to infect humans. VZV infections are species-specific to humans.
- It causes chickenpox (varicella), a disease most commonly affecting children, teens and young adults and herpes zoster (shingles) in older adults; shingles is rare in children. VZV is known by many names, including chickenpox virus, varicella virus, zoster virus, and human herpesvirus type 3 (HHV-3). hingles usually appears in a band, a strip, or a small area on one side of the face or body. It is also called herpes zoster. Shingles is most common in older adults and people who have weak immune systems because of stress, injury, certain medicines, or other reasons.Â
- VZV enters by inhalation and replicates in the mucosa of the respiratory tract. Dissemination occurs via bloodstream and lymphatics and the virus multiplies in mononuclear leukocytes and capillary endothelial cells.
- The cutaneous rash results from the multiplication of the virus in epithelial cells, Vesicles and ulcers ďŹrst appear in the mouth (usually on the palate and the tongue but also on the gingiva) followed by a cutaneous rash that spreads centrifugally from the head and the trunk Lesions in the mouth are painful whereas lesions on the skin are painless but itchy, which may lead to secondary bacterial infection and permanents scars
- EpsteinâBarr virus aďŹects over 90% of humans usually transmitted by oral secretions or blood. The virus replicates in epithelial cells or B cells of the oropharynx.
- In children ⌠Subclinical⌠Adults⌠Inf Mononucleosis⌠nfectious mononucleosis (IM), also known as mono, kissing disease, or glandular fever,
- Symptoms: fever, lymphadenopathy, Oral ulcers, Palatal patechia and less commonly gingival ulceration⌠Recommendations include drinking enough fluids, getting sufficient rest, and taking pain medications such as paracetamol (acetaminophen) and ibuprofen.
- EBV has also been associated to other diseases such as cancers nd auto-immune diseases (Thorley-Lawson and Gross, 2004). OHL appears as a raised, white, corrugated lesion that most often develops on the ventral-lateral aspect of the tongue and may be unilateral or bilateral
- Human cytomegalovirus is the most common cause of congenital and perinatal infections. About 10% of infants are infected by the age of 6 months following transmission from their mother through the placenta, during delivery or by breast feeding
- HCMV infects many diďŹerent epithelial cells, endothelial cells, smooth muscle cells, mesenchymal cells, hepatocytes, granulocytes and monocyte-derived macrophages
- HCMV is thus found in many body secretions including saliva, urine, semen and breast milk.
- HIV-infected patients, oral ulcers associated with HCMV have been reported (Scully and Porter, 1998) as well as gingival hyperplasia
- Thr are 6 type of Hep virus A,b,c,d,e,g in tht hepmB-dna virus while othr are rna genome
- Hepatitis A, once called âshort incubationâ or âinfectiousâ hepatitis, Non evloped Single stranded RNA virus,icosahedral symmetry Hepatitis A is common throughout the world. In the developing countries, the incidence of hepatitis A is very high due to overcrowding and poor sanitation. hepatitis A is rarely fatal and does not lead to chronic liver disease.
- Incubation period 2-6 wks⌠spread primarily by the fecal-oral route, either through person-to-person contact or ingestion of contaminated food or water. Transmission is often facilitated by poor personal hygiene, lack of sanitation, and oral-anal sexual contact. Common sources of contaminated food include shellfish, frozen raspberries and strawberries, and milk. can also be directly transmitted through transfusions of blood or blood products, although this is much less common due to the brief period of time that hepatitis A virus remains in the blood of an infected person infection among drug users is primarily due to poor hygiene rather than transmission through blood.
- Symptoms usually develop within 28 days after exposure. e fever, fatigue, poor appetite, nausea, and vomiting. Diarrhea occurs more commonly in children Cough, sore throat, runny nose and eyes, and arthralgias have been reported in some outbreaks Yelowish skin and eyes dark urine light stools
- DNA enveloped virus noncytopathic hepatotropic virus Hept B Can cause lifelong infection, cirrhosis (liver scarring), liver cancer, liver failure and death
- Professionals Injection drug users Sex partners of those with Hep B Sex with more than one partner homosexual Contact with blood Transfusions Dialysis
- Diagnostic tests Hbsag frst marker toappear in blood Hbeag to be an adverse prognostic sign Hbcag not detectabl in serum but detect in liver cell
- Passiv immunion.. Hyperimmune hepatitis B immune globulin ( HBIG) IM 300-500 i.u Active immunization Non glycosylated HBsAg particle ⌠IM 3 dosesâŚ0,1,6 months. Child born to carrier mothers 0.5ml of HBIG immediately after birth then the complete course first injection being given within 12 hrs of birth.
- Hepatitis B vaccines ..3 injections .. 6 months and Hepatitis A vaccines ..2 injections. Twinrix, which combines both the Hepatitis A and Hepatitis B vaccines and it includes only 3 injections.. protection against both Hepatitis A & B vaccines are very powerful and can provide long term protection against the disease.
- Used to be known as ânon-A, non-Bâ hepatitis Singl rna virus
- Hepatitis C is a contagious liver disease that results from infection with the Hepatitis C virus. It can range in severity from a mild illness lasting a few weeks to a serious, lifelong illness. Hepatitis C is usually spread when blood from a person infected with the Hepatitis C virus enters the body of someone who is not infected
- Sialadenitis is an infection of the salivary glands. The parotid and submandibular glands are most commonly affected. associated with pain, tenderness, redness, and gradual, localized swelling. Sjogren's syndrome is a disorder immune system -two most common symptoms â dry eyes and a dry mouth Oral lichen planus-inflammatory condition that affects mucous membranes in mouth. appear as white, lacy patches; red, lesions may cause burning, pain or other discomfort
- Alanine Aminotransferase Biopsy Provides useful information about the degree of fibrosis in HCV infected patients s not used for diagnosis of HCV infection.Used for assessment of severity of inflammation, presence of fibrosis, evaluate possible concomitant disease processes, assess therapeutic intervention. Histology Activity (necro-inflammation) â severity and progress
- There is no vaccine for Hepatitis C. The best way to prevent Hepatitis C is by avoiding behaviors that can spread the disease, especially injection drug users
- Hepatitis Delta VirusSingle stranded, self complementary RNA, encapsidated in HbsAg Small, amorphous particle RNA encodes one protein: delta antigen May be acquired as co-infection with HBV, or superinfection of HBV infection Occurs along with HBS.. Similar to itâŚSame injection HBV-coz delta antigen cant infect person immune to hbv
- Singl rna virus Clinically resembles hep a
- It is spherical enveloped virus it contains ,2 identicl copies of singl RNS,it hs revrse transcriptase enzyme,virus contain a lipoprotein envelope virus core surrounded by nucleocaspid of protein.,Major virus coded envelp glycoproteins r d projectin spikes on surface
- HIV has a strog affinity towards cells of immune system most specifically those carry cd4 cell surface recptor mostly effected,then aftr attaching ths cell virus Undergo replictn in the lymphoid tissues of lymph node,spleen,gut
- Homosexual and bisexual men illegal injection drugs hemophilia or other coagulation disorders Blood transfusion Infants of HIV-infected mothers
- Linear gingival erythema is defined as a distinct erythematous band of marginal gingiva with either diffuse or punctuate erythema of the attached gingiva. Persisent linear easily bleeding,,localised or generalized in nature,
- NG results in the destruction of one or more interdental papillae and remains confined to the marginal gingiva. increased incidence of NUG among HIV-infected individuals cleaning and debridement of affected areas with a cotton pellet soaked in peroxide after application of a topical anesthetic. An antimicrobial oral rinse, such as chlorhexidine gluconate 0.12%, is prescribed. Systemic antibiotics, such as metronidazole or amoxicillin, The use of prophylactic antifungal medication should be considered if antibiotics are prescribed.
- A necrotizing, ulcerative, rapidly progressive form of periodontitis occurs more frequently among HIV-positive individuals NUP is characterized by soft tissue necrosis, rapid periodontal destruction, and interproximal bone loss Occasionally patients undergo spontaneous resolution of the necrotizing lesions, leaving painless, deep interproximal craters that are difficult to clean and that may lead to conventional periodontitis. Therapy for NUP-local debridement,scaling and root planing, in-office irrigation with an effective antimicrobial agent, such as chlorhexidine gluconate or povidone-iodine (Betadine), and establishment of meticulous oral hygiene, including home use of antimicrobial rinses or irrigation
- Treatment for NUS may include an antibiotic, such as metronidazole, and use of an antimicrobial mouth rinse such as chlorhexidine gluconate. If osseous necrosis is present, it is often necessary to remove the affected bone to promote wound healing
- common in HIV-positive individuals and worsens as the viral load increases to more than 100,000 copies per mm3. Enlargement of the major salivary glands, particularly the parotids.
- recognising a pathophysiologyic relationship between mammalian viruses and PD disease has the potential to extend our insight into mechanism pD tissue braekdoen. Based on the current information it seems reasonable to add PD disease to list of infectious disease that have HCMV , EBV and other viruses as contributory causes