email antarleenasengupta@gmail.com for full seminar

1. ROLE OF VIRUSES IN
PERIODONTAL DISEASES
DR. ANTARLEENA SENGUPTA
I MDS, DEPTT OF PERIODONTOLOGY,
MCODS MANGALORE
2020.

2. CONTENTS
• INTRODUCTION
• EVOLUTION OF VIRUSES
• BALTIMORE CLASSIFICATION
• VIRAL COMPONENTS AND
STRUCTURE
• VIRAL REPLICATION
• HOST RESPONSE
• ACUTE INFECTIONS
• PERSISTENT INFECTIONS
• HIV
• HERPESVIRUSES
• PAPILLOMAVIRUSES
• PICORNAVIRUSES
• PARAMYXOVIRUSES
• CONCLUSION
• REFERENCES

3. INTRODUCTION
• VIRUS- infective agent that typically consists of a nucleic acid molecule in a protein coat,
is too small to be seen by light microscopy, and is able to multiply only within the living
cells of a host.
• Smallest living unit
• Viruses – first described – filterable agents
• “Living chemicals” – crystallised like chemicals – Stanley, 1935
• Extraction of “infectious nucleic acid” - Geirer & Schramm, 1956

4. EVOLUTION OF
VIRUSES
a. The ‘virus early’ hypothesis
assumes that viruses evolved
from early replicative elements
that preceded the first cellular
life forms.
b. The ‘regression’ hypothesis
suggests that viruses emerged
through the degeneration of
cells that then assumed a
parasitic lifestyle.
c. Finally, the ‘escaped genes’
hypothesis proposes that cellular
genes acquired the ability for
‘selfish’ replication and spread.

5. BACTERIA VIRUS
Intercellular organisms Intracellular organisms
SIZE Larger (1000 nm) Smaller (20-400 nm)
LIVING ATTRIBUTES Living organism
STRUCTURES DNA and RNA floating freely in
cytoplasm. Has cell wall and cell
membrane
DNA or RNA enclosed inside a coat
of protein
RIBOSOMES Present Absent
REPRODUCTION Fission– a form of asexual
reproduction
Invades host cell and takes over the
cell causing it to make copies of the
viral DNA/RNA. Destroys the host
cell releasing new viruses
TREATMENT Antibiotics Vaccines prevent the spread and
antiviral medications help to slow
reproduction but can not stop it
completely

6. BALTIMORE CLASSIFICATION (1971)
- Classification system that places viruses
into one of seven groups
- depending on a combination of
i. their nucleic acid (DNA or RNA)
ii. strandedness (single-stranded or
double-stranded)
iii. Sense
iv. method of replication.
- Designated by Roman numerals.

7. BALTIMORE CLASSIFICATION (1971)

8. VIRAL COMPONENTS AND STRUCTURE
• Virion –is a complete virus particle consisting of RNA or DNA surrounded
by a protein shell, constituting the infective form of virus
i. Genome - either DNA or RNA but not both
ii. Capsid
iii. Envelope
iv. Peplomers
v. Enzymes

9. CAPSID
• Shell made of protein building blocks or promoters
• Self assemble into larger capsomere – then into virion capsid
• Simplest structures - symmetrical
i. Helical – form rods
ii. Icosahedral – approximation of a sphere

10. ENVELOPE
• Similar to cellular membranes
• Consists of lipids , proteins and glycoproteins
• Glycoproteins – extend from surface , act as virus attachment
• Proteins (VAP) , are major antigens for protective immunity

11. VIRUS REPLICATION

12. HOST RESPONSE
[I] ANTIBODY MEDIATED ANTIVIRAL IMMUNITY
a) Viral Antibodies :
• IgG – block adsorption and penetration into host cells
• Enhance ingestion by PMNs and macrophages
• Agglutinate the virus – reduce viral load
• Ag – Ab complex - increase size to trigger phagocytosis

13. b) Antibodies with activation of complement system
• Generation of C3 –viral Ab complex allows binding of C3 receptor –
phagocytosis
• Ab and Complement – lysis of virus with envelope – damage lipid membrane
• - Lysis of infected cells
• Complement alone – activate alternate pathway – lysis or increased
phagocytosis of coated material
c) Ig bound to virus infected cell interacts with Fc receptor
• bearing lymphocytes (K cells) – cell lysis

14. II] CELL MEDIATED ANTIVIRAL IMMUNITY

15. III] NON SPECIFIC FACTORS
1. Fever
2. Interferon Production
3. Natural Killer Cell Activity

16. ACUTE INFECTIONS
• Events that contribute to cytopathic changes & cell death
1) Inhibition of host cell DNA , RNA and protein synthesis
2) Virion proteins
3) Activation of lysosomal enzymes
4) Inhibition of Na+-K+ pump

17. PERSISTENT INFECTIONS

18. INTERFERON
• Innate mechanism
• Group of peptides – bind to receptors of neighbouring cells - resistant to infection -
limiting focus of infection
• Regulate cell differentiation and immune reactivity
• IFN α – T lymphocytes
• IFN β – virus stimulated fibroblasts
• IFN γ- most potent , Ag activated T cells. Stimulates macrophages to
elaborate t-cell-activating cytokines.

19. RETROVIRUS

20. HUMAN IMMUNODEFICIENCY VIRUS
• Retrovirus
• HIV 1
• HIV 2
• 1981 – first indication of AIDS in NY and LA
• 1983 – Luc Montagnier et al isolated retrovirus and called it LAV – lymphadenopathy
associated virus
• 1984 – Robert Gallo – HTLV III – Human T cell lymphotropic virus III
• 1985 -- ELISA
• 1986 – International committee of Virus Nomenclature - HIV

21. STRUCTURE

22. VIRAL GENES AND ANTIGENS
- gag
- pol
- env
- tat (trans activating gene)- enhances expression of all viral genes
- net (negative factor gene)- downregulates viral replication
- rev (regulator of virus gene)- enhances expression of structural
proteins
- vif (viral infectivity factor gene)- influencing infectivity of viral
particles
- vpu (only in HIV I) & vpx (only in HIV II)- enhances maturation and
release of progeny virus from cells (distinguish between HIV 1 and 2)
- vpr- stimulating the promoter region of the virus
- LTR (long terminal repeat) sequences- one at either end, containing
sequences giving promoter, enhancer and integration signals

23. PATHOGENESIS
• Receptor for the virus is CD4
• Primary CD4+
• T lymphocytes (helper/inducer)
• 5-10% of B lymphocytes
• 10-20% of monocytes and macrophages
• Specific binding to CD4 receptor - envelope glycoprotein
gp120.
• Cell fusion - trans membrane gp41.
• CXCR4 for T cell tropic HIV
• CCR5 for macrophages –co-receptors

24. VIRUS ATTACHMENT &
PENETRATION
- Viral attachment and penetration: the phage infects a
cell
- Integration: the phage DNA becomes incorporated into
the host genome
- Excision: the phage is excised from the bacterial
chromosome alongwith a short piece of bacterial DNA.
The DNA is then packaged into newly formed capsids
- Infection: phage containing both viral and bacterial
DNA infect a new host cell
- Recombination: the phage DNA, alongwith the
attached bacterial DNA are incorporated into the new
cell

25. PERIODONTITIS AND HIV REACTIVATION
• Immune and oral epithelial cells latently
infected with HIV in gingival tissues--
important source for HIV reactivation
• IL-1, TNF-α activate nuclear factor kappa B
[NFκB]-- induce viral gene expression
through interaction with LTR of the HIV
provirus
• IFN-γ, IL-6 & TNF-α up-regulate IRF-1
• cell activation
• drives HIV-1 replication
• Inflammatory mediator PGE2
• IL-2 and IL-7 Proposed model of HIV reactivation during co-
infection
[UPPOOR AND NAYAK, 2012]

26. -
- This damage is caused to CD4+ T cells.
- ↓T4 cells and T4:T8 ratio is reversed.
Suppress function of infected cells without causing structural
damage.
- T4 cells do not release IL2, IFN, and other lymphokines
MONOCYTE –
MACROPHAGE FUNCTION
HUMORAL
MECHANISM
PATHOGENIC MECHANISM
•Helper T cell activity is essential for optimal B cell
function
•Hypergammaglobulinemia is more a hindrance than
help because of ‘USELESS Ig’ to irrelevant Ags and also
autoantibodies.
• Affected due to lack of secretion of activating factors by T4
lymphocytes.
•So chemotaxis, antigen presentation and intracellular killing is
diminished.
•Activity of NK cells and cytotoxic T cells is affected

27. CLASSIFICATION OF CLINICAL
MANIFESTATIONS
• Group I : Acute Infection
• Group II : Chronic Asymptomatic Infections
• Group III : Persistent Generalized Lymphadenopathy
• Group IV : AIDS- Related Complex

28. CLASSIFICATION OF CLINICAL MANIFESTATIONS

29. CLASSIFICATION OF CLINICAL MANIFESTATIONS
CHRONIC ASYMPTOMATIC INFECTIONS
• Most dangerous group
• Seropositive patient who is apparently healthy capable of infection
• Enlarged axillary glands
• Hematological & immunological abnormalities

30. CLASSIFICATION OF CLINICAL MANIFESTATIONS
CHRONIC ASYMPTOMATIC INFECTIONS
• Most dangerous group
• Seropositive pt who is apparently healthy capable of infection
• Enlarged axillary glands
• Hematological & immunological abnormalities

31. CLASSIFICATION OF CLINICAL MANIFESTATIONS
• PERSISTENT GENERALISED LYMPHADENOPATHY
• LYMPHADENOPATHY in 2 or more extrainguinal sites persisting for
more than 3 months

32. CLASSIFICATION OF CLINICAL MANIFESTATIONS
• AIDS-RELATED COMPLEX
• OPPORTUNISTIC INFECTIONS
• -Pneumonia, Cryptococcosis,
• Viral Infections, Toxoplasmosis, TB etc.
• NEOPLASMS
• KS, Lymphoma, SCC
• NEUROLOGIC DISEASES
• - Meningocephalitis
• OTHERS
• Encephalopathy, Purpura,
Thrombocytopenia

33. LINEAR GINGIVAL ERYTHEMA (HIV-G)
• A persistent , linear , easily bleeding,
erythematous gingivitis
• Possible etiology – Candida dubliniensis
• Prevalence in HIV patients – 0-49%
• May be localized or generalized
• No evidence of pocketing or attachment
loss
[GP Moran, 2012]

34. NECROTISING ULCERATIVE GINGIVITIS
PERIODONTITIS , STOMATITIS
• NUG – destruction of 1 or more interdental papilla;
confined to marginal gingiva
• NUP- involves PDL and alveolar bone. Bone is exposed
– necrosis – sequestration
• NUS – extends past MGJ into mucosa and osseous
tissues
• Higher prevalence in HIV patients
• NUP – marker of immune deterioration with 95%
predictive value
• Prevalence of Chronic periodontitis – 5-69%

35. HERPESVIRUSES

36. HERPES VIRUSES
- Membership in the family
Herpesviridae is based on four
layered structure of the virion.
- Herpesviruses have
i. A core contaiing a large double
stranded DNA genome encased
within
ii. An icosapentahedral capsid
containing 162 capsomers
iii. An amorphous proteinaceous
tegument
iv. Surrounding the capsid and
tegument, a lipid bilayer envelope
derived from host cell membranes

37. CLASSIFICATION
α β γ
HSV 1
HSV 2
VZV
CMV
HHV 6
HHV 7
EBV
HHV 8

38. HERPESVIRUS LIFE CYCLE
Virion particle recognizes and attaches to surface
receptors of the mammalian cell
Viral penetration into the cell
Transcription of viral mRNA, viral protein synthesis,
and replication of the viral genome
Viral genome and structural proteins assembled
Virions are released from the cell by exocytosis or by
cell lysis

39. VIRUS REPLICATION
Attachment and
penetration by fusion
Immediate early
Protein synthesis
Early protein synthesis and
genome replication
Late protein synthesis
exocytosis and release
Assembly and release
Lysis and release
LATENT
ACTIVE

40. VIRUS REPLICATION
Replication in epithelial cells
Viral nucleocapsids ascend local sensory neurons by retrograde
axonal transport
Establish lifelong latency in corresponding spinal or cerebral
ganglion
Reactivation occurs at any time
Virus replication in infected neurons
Virus transported down the axon to original position

41. 1. Direct cytopathic effects
2. Impair cells involved in host defense
3. Promote subgingival attachment and colonization
4. Altered inflammatory mediator
5. Reducing the cell surface expression of MHC class I molecules
MECHANISMS OF PERIODONTOPATHIC
POTENTIAL OF HERPES VIRUSES
- Fibroblasts, keratinocytes, endothelial cells, on
inflammatory PMNLs and macrophages, and
possibly on bone cells
- Hamper tissue turnover and repair.
- Predisposing to microbial superinfection.
- HCMV and EBV-1
- infect and/or alter functions of monocytes,
macrophages and lymphocytes.
- Subgingival attachment and
colonization of
periodontopathic bacteria
- Viral proteins -- act as
bacterial receptors and
generate new bacterial
binding sites.
- provide new sites for
bacterial binding.
- Altered inflammatory mediator and
cytokine responses.
a.HCMV  upregulate IL- 1β and TNF-α
gene expression of monocytes and
macrophages which upregulate MMPs,
downregulate tissue inhibitors of
metalloproteinase and mediate
periodontal bone destruction.
b.- EBV-mediated transformation of B-
lymphocytes to plasma
- particularly prominent in progressive
periodontitis lesions
HCMV and HSV induce cell-mediated
immunosuppression
- ↓Cell surface expression of MHC class
I molecules
- interferes with T-lymphocyte
recognition.
- cause metabolic abnormalities in
lymphocytes and monocytes
- suppress antigen-specific cytotoxic T-
lymphocyte functions
- decreased circulating CD4+ cells
- Increased CD8+ suppressor cells

42. HERPESVIRAL–BACTERIAL INTERACTIONS IN
PERIODONTAL DISEASES
[SLOTS et al., 2010],
PERIODONTOLOGY 2000
B cells with
latent EBV
Macrophages
with latent HSV
& CMV
T cells with
latent HSV
&CMV
PERIODONTOPATHIC
PROPERTIES
HERPESVIRUS
ACTIVATION
GINGIVITIS
BACTERIAL BIOFILM
HEALTHY GINGIVA
1. IMMUNOSUPRESSION
FROM INFECTION OR
CYTOTOXIC THERAPY
2. INFLAMMATION
3. PSYCHOSOCIAL STRESS
OR NUTRITIONAL STRESS
4. HORMONAL CHANGES/
PREGNANCY
5. PHYSICAL OR
CHEMICAL TISSUE
INJURY
6. TOBACCO USAGE
7. AGING
8. OTHERS

43. PRIMARY HERPETIC GINGIVOSTOMATITIS
• HSV- type 1
• Infants/ children younger than 6
yrs
• Males=females
• Primary infection asymptomatic
• The virus ascends through the
sensory or autonomic nerves and
persists in the neuronal ganglia
that innervate the site as a latent
HSV
• Sunlight, fever, trauma, stress ,
after oral surgical procedures
Secondary manifestations
• Herpes labialis
• Herpetic stomatitis
• Herpes genitalis
• Ocular herpes
• Herpetic encephalitis

44. PRIMARY HERPETIC GINGIVOSTOMATITIS
• INTRA ORAL
 Diffuse, erythematous, shiny involvement of the gingiva
and adjacent oral mucosa
 Varying degree of edema and gingival bleeding
 Discrete spherical grey vesicles
 Rupture of vesicles and formation of ulcers after 24 hrs
 Ulcers– small , painful, red, elevated, halo-like margin
with depressed yellowish/greyish white central portion
 An important diagnostic criteria in this disease is the
appearance of a generalized acute marginal gingivitis
 Widely spread/clusters
 7-10 days
 No scarring
CLINICAL FEATURES

45. PRIMARY HERPETIC GINGIVOSTOMATITIS
 Soreness, difficulty in eating and
drinking
 Ruptured vesicles sensitive to touch,
thermal changes, foods such as
condiments and fruit juices
 Infants show irritability and refusal to
take food
CLINICAL FEATURES

46. PRIMARY HERPETIC GINGIVOSTOMATITIS
EXTRA ORAL
 Cervical adenitis
 Fever (101-105 deg F)
 Generalized malaise
CLINICAL FEATURES

47. PRIMARY HERPETIC GINGIVOSTOMATITIS
 Early diagnosis– important (reducing symptoms and recurrences)
 History/clinical findings
 Virus culture
 Immunologic tests using monoclonal antibodies or DNA
 Hybridization techniques
 Most commonly used diagnostic procedures – cytological smear &
tissue biopsy
DIAGNOSIS

48. PRIMARY HERPETIC GINGIVOSTOMATITIS
COMMUNICABILITY
Contagious
Most adults develop immunity due to infection during childhood –
subclinical infection
Hence seen in infants & children
Studies have demonstrated HSV in periodontal pockets (Slots J,
2000)

49. PRIMARY HERPETIC GINGIVOSTOMATITIS
TREATMENT
• Consists of early diagnosis & immediate initiation of antiviral therapy.
• 1. Antivirals :
- Acyclovir suspension 15mg/kg is given 5 times daily for 7 days (Amir et
al,1997)
- It reduces days of fever, pain, lesion and virus shedding
- Acyclovir does not affect normal cells but inhibits DNA replication in HSV
infected cells
- Newer antivirals like Valacyclovir and Famicyclovir can also be used
• <3 days– antiviral
• >3 days- (immunocompetent pt) limited value

50. PRIMARY HERPETIC GINGIVOSTOMATITIS
TREATMENT
• 2. Palliative measures:
- Removal of food debris, plaque and supragingival calculus
• NSAID (FEVER AND PAIN)
• Extensive periodontal therapy to be postponed
• Local /systemic antibiotics to prevent opportunistic infection especially in
immuno-compromised patients
• The patient must be informed that the disease is contagious, thus precautions
must be taken (VESICLES – HIGHEST VIRAL TITER)

51. PRIMARY HERPETIC GINGIVOSTOMATITIS
TREATMENT
• 3. Supportive measures:
Copious fluid intake
Nutritional supplements
Topical anesthetics while eating
Infection of fingers of health professional
treating infected patients– HERPETIC
WHITLOW

52. VARICELLA ZOSTER VIRUS
- causes varicella (chicken pox) as the primary
self‐limiting infection.
- Mainly in children
- Later reactivation of the virus in adults herpes
zoster (shingles). Aka Ramsay Hunt’s Syndrome
- Both manifestations can involve the gingiva (Scully,
1995).
- C/F:
- Fever
- Malaise
- skin rash.
- Intraoral lesions: small ulcers usually on the tongue,
palate, and gingiva (Scully et al. 1998).

53. VARICELLA ZOSTER VIRUS
- The virus remains latent in the dorsal root ganglion from where it can be reactivated
years after the primary infection (Rentier et al. 1996).
• Later reactivation herpes zoster, with unilateral lesions following the infected nerve
(Miller, 1996). Lesions similar to varicella but remain confined to single dermatome
and are unilateral
- Initial symptoms-- pain and paraesthesia
- Start as vesicles-- soon rupture to leave fibrin‐coated ulcers, which later coalesce.
- Immunocompromised patients, including those infected with HIV, the infection can
result in severe tissue destruction with tooth exfoliation and necrosis of alveolar bone
and high morbidity (Schwartz et al. 1989).
- Healing of the lesions usually takes place in 1–2 weeks.
- Treatment consists of a soft or liquid diet, rest, atraumatic removal of plaque, and
diluted chlorhexidine rinses. This may be supplemented by antiviral drug therapy.

54. EPSTEIN-BARR VIRUS (HHV type IV)
- 1964 - African Burkitt lymphoma.
- Infects epithelial cells with a cytolytic infection and B lymphocytes(oropharynx) with a latent infection.
• Transmitted by oral secretions or blood.
• All seropositive patients- actively shed virus in saliva.
• Resting memory B cells –main site of persistence of EBV.
• EBV infection – in children is subclinical, in adults- infectious mononucleosis.
- Recurrent aphthous stomatitis
- Erythema multiforme
- Lymphoepithelioma
- Warthin’s tumor
- Oral SCC
- Tonsillar carcinoma
- Lymphoid tumors (Hodgkin’s/Non-Hodgkin’s)

55. ORAL HAIRY LEUKOPLAKIA
• Main lesion of EBV
• Non malignant hyperplastic lesion of
epithelial cells which shows non-cytolytic
EBV replication.
• appears as white corrugated lesion on
ventrolateral aspect of tongue
• may be unilateral/bilateral.

56. ORAL SQUAMOUS CELL CARCINOMA
• Epstein-Barr virus (EBV) -- associated
with malignant cell transformation
• ↓Latent membrane protein-1 (LMP-
1) ++→ oncogenic transformation of
B lymphocytes and the appearance of
lymphoproliferative processes
• Transform human fibroblasts and
keratinocytes.
• Activation of transcription factors NF-
κB, activator protein (AP)-1
Gupta AA (2015) Unconventional Causes of Conventional Oral Cancer. J Clin Exp Pathol

57. KAPOSI’S SARCOMA
• Human gammaherpesvirus 8
• HIV+ individual with Kaposi’s AIDS
• Malignant
• Predominantly in homosexuals.
• Angioproliferative tumor
• Lesions are vascular, angiomatous neoplasms that begin
as red macule & progress to large tumefactive red &
purple lesions.
• Oral lesions: multifocal & typically seen on palate &
gingiva
• Presently oral Kaposi's sarcoma is primarily treated with
systemic and intralesional chemotherapy,
immunotherapy, radiation, and occasionally lasers.

58. HUMAN CYTOMEGALOVIRUS (hCMV)- HHV V
• Infects mainly T-lymphocytes and macrophages
• The gB protein in the virion envelope participates in the virus-cell interaction and is a major
target of the immune response
• Most common cause of congenital and perinatal infections.
• Infants infected through placenta, during delivery or breastfeeding.
• Infects epithelial cells, endothelial cells, smooth muscle cells, mesenchymal, hepatocytes,
granulocytes, macrophages.
• Found in saliva, urine, semen, breast milk.
• In HIV infected patient-oral ulcers as well as gingival hyperplasia is noted.
• HIV/AIDS related oral ulcers
• Recurrent aphthous stomatitis
• Kaposi’s sarcoma
• Mononucleosis

59. ROLE OF hCMV IN PERIODONTAL DISEASE
Cells
Monocytes, Macrophages
T-lymphocytes
Shedding via GCF
Stimulus
Plaque-induced inflammation
Stress, cigarette smoking
Latency infected
Released through GCF
latency
Reactivation
HCMV infected Gingival connective tissue
Inflammatory cells
Monocytes
Macrophages
Gingival fibroblast
Metalloproteinases
Up-regulation mRNA
Expression MMP1 & 2
Immune invasion
Inhibition apoptosis
MHC-1 downregulation
Cytokine overproduction
IL-1b, TNF, IL-8
Collagen alteration
Downregulation mRNA
expression collagen I & III
Loss of connective tissue & bone tissueGupta C, Dhruvakumar D. Role of periodontopathogenic virus in periodontal disease: a
review. Tanta Dental Journal. 2017

60. SLOTS, 2010, Perio 2000

61. PAPILLOMAVIRUS

62. HUMAN PAPILLOMA VIRUS
• Group of small, epitheliotropic, non-
enveloped, icosahedral, ds circular
DNA viruses
• >100 varieties
• Benign skin lesions (warts)
• Type 16 HPV– oropharyngeal SCC

63. ROLE OF HPV IN ORAL CANCER
• HPVDNA generally is integrated into the host genome.
• Integration of HPVDNA disrupts or deletes the E2
region, which results in loss of its expression.
• The HPV E6 gene product binds to p53 and targets it for
rapid degradation
• As a consequence, the normal activities of p53 which
govern G1 arrest, apoptosis, and DNA repair are
abrogated.
• The HPV E7 gene product binds to pRb and this binding
disrupts the complex between pRb and the cellular
transcription factor E2F-1, resulting in the liberation of
E2F-1, which allows the transcription of genes whose
products are required for the cell to enter the S phase
of the cell cycle
Gupta AA (2015) Unconventional Causes of Conventional Oral Cancer. J Clin Exp Pathol
In the oral cavity, periodontitis has been
associated with papillomavirus-16-related
squamous cell carcinoma of the tongue. Co-
infection with papillomavirus-18 and Epstein–
Barr virus has also been linked to tongue
carcinoma. As periodontitis lesions frequently
harbor papillomaviruses, and may even
comprise the major oral reservoir of the virus,
periodontitis sites in intimate contact with the
tongue may serve as the source of oncogenic
papillomaviruses.

64. PICORNAVIRUS

65. PICORNAVIRUS
- Coxsackievirus
- Echovirus
- Enterovirus
- Closely related with pathogenesis
of hand, foot and mouth disease
- Symmetric icosahedral capsid
- 60 protomeres (VP1, VP2,
VP3…….)

66. HERPANGINA
• Coxsackie group A virus
• Ingestion, contact, droplet
• Seen in summer, in young
• Symptoms – sore throat, cough,
rhinorrhea, fever, vomiting and even
abdominal pain
• Vesicles which rupture to form ulcers
• All of these heal by 7 days
• No treatment needed as it is self
limiting

67. HAND, FOOT AND MOUTH DISEASE
• Coxsackie and entero virus
• Multiple ulcers with dysphagia
• Intracytoplasmic viral inclusions, high
antibody titer to Coxsackie
• Self limiting

68. PARAMYXOVIRUS

69. PARAMYXOVIRUS
• Paramyxovirus: One of a group of RNA
viruses that are predominantly
responsible for acute respiratory
diseases and are usually transmitted
by airborne droplets.
• The paramyxoviruses include the
agents of mumps, measles (rubeola),
RSV (respiratory syncytial virus),
Newcastle disease, and parainfluenza.
- enveloped particles
- 150 to 300 nm in diameter.
- tubelike, helically symmetrical nucleocapsid
- contains a monopartite, single-stranded,
negative-sense RNA genome and an RNA-
directed RNA polymerase.
- The nucleocapsid associates with the matrix
protein (M) at the base of a double-layered
lipid envelope.
- The spikes on the envelope contain two
glycoproteins, a viral attachment protein,
and a fusion protein.

70. RUBEOLA (Measles)
• Produced by a paramyxovirus
• Affected individuals are infectious from 2 days
before becoming symptomatic until 4 days after
appearance of the rash
• Incubation period of 8 to 12 days
• Pre eruptive, eruptive and post eruptive stages
• Small red macules or papules appear which
enlarge and coalesce to form
• irregular lesions which blanch on pressure and
gradually fade in 4 or 5 days.
• Koplik’s Spots
• Warthin Finkeldey giant cells

71. RUBELLA (GERMAN MEASLES)
- Capacity to induce birth defects
• Forchheimer spots- small discrete dark-red
papules that develop on the soft palate and
may extend onto the hard palate capacity to
induce birth defects
• FORCHHEIMER’S SPOTS aka pathognomonic
sign for Rubella.

72. EPIDEMIC PAROTITIS (MUMPS)
• Mumps affects the parotid glands, salivary glands below and in front of
the ears. The disease spreads through infected saliva.
• Some people experience no symptoms. When symptoms occur, they
include swollen, painful salivary glands, fever, headache, fatigue and
appetite loss.
• Treatment focuses on symptom relief. Recovery takes about two weeks.
The disease can be prevented by the MMR vaccine.
How it spreads
• By airborne respiratory droplets (coughs or sneezes).
• By saliva (kissing or shared drinks).
• By touching a contaminated surface (blanket or doorknob).
• Consult a doctor for medical advice

73. CONCLUSION
Several studies, most of them from the same research group, have demonstrated an
association of herpes viruses with periodontal disease.
Viral DNA has been detected in gingival tissue, GCF and subgingival plaque from periodontally
diseased sites. In addition, markers of herpes viral activation have also been demonstrated in
the GCF from periodontal lesion. Active hCMV reactivation triggers periodontal disease
activity.
Studies have documented an association between chronic periodontitis and viral
microorganisms of the herpesvirus group, most notably Epstein-Barr virus-1 (EBV-1) and
human cytomegalovirus (HCMV). Further, the presence of subgingival EBV-1 and HCMV are
associated with high levels of putative bacterial pathogens, including P. gingivalis, T. forsythia,
P. intermedia, and T. denticola. These data support the hypothesis that viral infection may
contribute to periodontal pathogenesis, but the potential role of viral agents remains to be
determined.

74. REFERENCES
• Textbook of Clinical Periodontology, 13th edition- CARRANZA
• Textbook of clinical periodontology & Implant dentistry, 7th Edition- LINDHE
• Textbook of Microbiology 7th Edition PANIKER
• Jorgen slots. Human viruses in periodontitis Perio 2000, Vol. 53, 2010, 89–110
• I Cappuyns, P Gugerli, A Mombelli . Viruses in periodontal disease – a review Oral Diseases
2005, 11, 219–229
• Slots J: Oral viral infections of adults. Periodontol 2000 49:60, 2009.
• Gupta, Chandni & Arun, Deepa. (2017). Role of periodontopathogenic virus in periodontal
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75. THANK YOU.