INTRODUCTION
Virus is a Latin word which means venom or poison. The size of the viruses
varies in millimicrons.
It
consist of central core of DNA or RNA.Virally infected cells produce the same type of
nucleic acid so susceptibility of cells infection may be increased. Viruses cause
certain infectious diseases and produce long-lasting immunity against
reinfection by the same virus.
In addition , there are many neoplasm can be caused
due to the viral infection. The classification of virus is difficult because of
size of viruses and their incompletely understood metabolic systems. However,
their classification based on biologic, chemical and physical properties of the
animal viruses, separating them into groups according to the type of nucleic
acid, and the size, shape and substructure of particle has been undertaken by
the International Committee on Nomenclature of Viruses of the International
Association of Microbiological Societies.
CLASSIFICATION OF MAJOR VIRUS GROUPS AND DISEASE
DNA VIRUS RNA VIRUS
A) Herpes
Virus
1) Herpes Simplex
2) Varicella/ herpes zoster
3) Cytomegalic/ inclusion disease
4) Epstein- Barr Virus
−
Infectious
Mononucleosis
B) Pox
Virus
1) Small Pox
2) Molluscum Contagiosm
C) Adeno
Virus
1) Pharyngo Conjunctival Fever
2) Epidemic Kerato conjuntivitis
D) Parvo
Virus
E) Irido Virus
F) Papova
Virus
1)Human
Warts or Papillomas
2) Tumorogenic Viruses
|
A) Orthomyxo
Virus
1) Influenza
B) Paramyxo
Virus
1) Measles
2) Mumps
C) Rhabdo
Virus
1) Rabies
2) Hemorrhagic fever
D) Arena Virus
1) Lymphocytic
Choriomeningitis
2) Lassa Fever
E) Calci Virus
F) Coona Virus
1) Upper Respiratory Infection
G) Bunya
Virus
H) Picorna
Virus
1) Poliomyelitis
2) Coxsackie disease
3) Common Cold
4) Foot & Mouth Disease
5) Encephalomyocarditis
I) Reo
Virus
T) Toga
Virus
1) Rubella
2) Yellow fever
3) St. Lovis Encephalitis
K) Retro
Virus
( RNA Tumour Virus )
|
HERPES SIMPLEX INFECTION
The Herpes simplex virus (HSV) – DNA virus. It bbelongs to
human herpes virus (HHV) family, also called Herpetoviridae. Other members
of this family are varicella-zoster virus, Epstein-Barr virus, Cytomegalovirus
etc. Humans are only known natural reservoirs and can stay
in the host for life and become periodically reactivated.
TYPES OF HSV
·
Herpes simplex virus – 1: This spread
through saliva. The lesions above
the waist, in oral, facial and ocular areas including pharynx, and skin.
·
Herpes simplex virus – 2: This transmitted
through sexual contact. It involves genitalia and skin below the waist.
PATHOGENESIS
Herpes Simplex virus infections are
seen in patterns . They are :
·
Primary infection: -This is initial exposure to virus, no antibodies are produced. It commonly occurs
in young age, often asymptomatic. The virus
taken up in sensory nerves and transported to associated ganglia.
·
Secondary infection: - It also known as recurrent infection. The virus can residing in ganglia reactivated. It is not always symptomatic; sometimes
patients only shed the virus through saliva.
The
predisposing factors for reactivation of virus are old age, UV light, emotional stress, trauma, menstruation,
systemic diseases or malignancy .
PRIMARY HERPETIC
GINGIVOSTOMATITIS
The primary
herpetic gingivostomatitis is a relatively common viral infection of the oral mucosa.
The herpes simplex virus could be isolated from patients with a particular
clinical configurations.
The etiology
for primary herpetic gingivostomatitis are Herpes simplex virus type 1 and Herpes simplex virus type 2 .
CLINICAL FEATURES
The age incidence of this viral infection is 6 months –
5 years . The sex
incidence is nil. The site
predilection are affects
movable and immovable mucosa , primarily gingiva, labial mucosa, vermilion
zone, palate. The onset of the disease is abrupt.
Primary herpetic gingivostomatitis is
clinically characterized by high fever ,headache, malaise, anorexia
,irritability ,bilateral sensitive regional lymphadenopathy ,sore mouth
lesions. The affected mucosa is red and edematous, with numerous coalescing vesicles,
which rapidly rupture, leaving painful small, round, shallow ulcers covered by yellow fibrin
New lesions continue to develop during the first three to five days. The ulcers
heal in 10–14 days. Both the movable and non movable oral mucosa may be
affected. Gingival lesions are almost always present, resulting in enlargement
and edematous and painful erosions. The diagnosis is usually made on clinical
grounds.
Primary herpetic gingivostomatitis: multiple ulcers on the tongue
LABORATORY
TESTS
Viral isolation from tissue culture inoculated
with the fluid of in tact vesicles is the most
definitive diagnostic procedure. The
serologic tests for HSV antibodies are positive 8 days after the initial
exposure. These antibody titres are useful in documenting past exposure and are
used primarily in epidemiologic studies. Two of the most commonly used
diagnostic procedures are the cytologic smear and tissue biopsy, with cytologic
study being the least invasive and most cost effective.
DIFFERENTIAL DIAGNOSIS
Aphthous ulcers, hand-foot-and-mouth
disease, herpangina,
acute necrotizing ulcerative gingivitis, erythema multiforme, early pemphigus,
desquamative gingivitis.
TREATMENT
Mainly symptomatic treatment and in
severe cases the systemic Acyclovir or
Valaciclovir can be given.
SECONDARY HERPETIC
STOMATITIS
Recurrent herpetic stomatitis is usually
seen in adult patient and manifests itself clinically as an attempted form of
the primary lesion.
ETIOLOGY
The secondary or recurrent herpetic
stomatitis is a relatively common oral and perioral disease that is due to
reactivation of HSV1. It
is commonly precipitated by fever, trauma, cold, heat, sunlight, emotional
stress, and HIV infection.
Secondary herpetic stomatitis:
small round ulcers on the palate
CLINICAL FEATURES
The most
common sites of recurrence for HSV-1 are lips and perioral skin , palate, attached
gingiva. Clinically,
the lesions present as multiple small vesicles arranged in clusters .The
vesicles soon rupture, leaving small ulcers that heal spontaneously within 6–10
days. The prodromal
symptoms are burning, itching, tingling, and erythema. Characteristically,
fever, generalized regional lymphadenopathy ,and constitutional symptoms are absent.
The diagnosis is made on clinical grounds.
DIFFERENTIAL DIAGNOSIS
Aphthous
ulcer, primary and secondary syphilis, streptococcal stomatitis, herpangina .
TREATMENT
The
symptomatic treatment is required.
HERPETIC WHITLOW
This are less common presentation , mainly
infection of fingers, and thumb. It
occurs due to self inoculation in children with orofacial HSV. It can also
occur in medical and dental professionals who do not wear gloves and come in
contact with infected patients.
HERPANGINA
The herpangina is an acute self-limiting viral infection,
also known as aphthous pharangitis or vesicular pharangitis . Most
cases arise in the summer or early fall in nontropical areas with crowding and poor hygiene aiding their
spread. The faecal-oral route is considered the major path of transmission, and
frequent hand washing is emphasized in an attempt to diminish spread during
epidemics.
ETIOLOGY
Usually
caused by coxsackievirus group A, types 1–6, 8, 10, and 22, and less commonly
by other types.
CLINICAL FEATURES
The
age incidence are commonly in children ,
occasionally in adult The incubation
period of 2-10 days The disease
presents with an acute onset of fever, sore throat, dysphagia, headache, and malaise, followed by
diffuse erythema and vesicles. The vesicles are small and numerous, and rupture
rapidly, leaving painful ulcers that heal within 7–10 days .
ORAL MANIFESTATION
Characteristically, the lesions appear
on the soft palate and uvula, tonsillar pillars, and posterior pharyngeal wall.
DIFFERENTIAL DIAGNOSIS
The herpetiform ulcers, aphthous
ulcers, primary herpes simplex infection, acute lymphonodular pharangitis,
erythema multiforme, FAPA syndrome, hand-foot-and-mouth disease.
TREATMENT
The supportive treatment is needed.
ACUTE LYMPHONODULAR PHARYNGITIS
The
acute lymphonodular pharangitis is an acute febrile disease caused by
strains of coxsackie virus A 10. It marked resemblance with herpangina .
CLINICAL FEATURES
This viral disease affect mainly in children and
young adult. The incubation period of 2-10 days. The chief complaints are sore throat, an elevation
of temperature, mild headache, anorexia.
ORAL MANIFESTATION
The raised , discrete , whitish or
yellowish to dark pink solid papules or nodules can be seen. It is surrounded by
narrow zone of erythema. The main sites are uvula, soft palate, anterior
pillars, posterior oropharynx .
LABORATORY FINDINGS
The primary
isolation of Coxsackie A10 Virus is main laboratory finding.
HISTOLOGIC FEATURES
The hyperplastic lymphoid aggregates in papules
or nodules can seen.
TREATMENT
No treatment required for this viral infection.
HAND-FOOT-AND-MOUTH DISEASE
Hand-foot-and-mouth
disease is an acute self-limiting contagious viral infection transmitted from
one individual to another.
ETIOLOGY
The main
etiology is Coxsackievirus strain A16, and rarely other strains.
CLINICAL
FEATURES
The disease
usually affects children and young adults, and often occurs in epidemics. Skin
lesions are not constant, and present as small vesicles with a narrow red halo.
The lateral borders and the dorsal surfaces of the fingers and toes are the
most common areas involved. The lesions may appear on the palms, soles, and buttocks.
The disease lasts five to eight days.
ORAL MANIFESTATIONS
It characterized by small vesicles and 5–30 in
number. It rapidly rupture, and leaving painful, shallow ulcers with diameter
2–6 mm and they are surrounded
by a red halo. The buccal mucosa, tongue, and labial mucosa are the most commonly
affected sites. The diagnosis is made on the basis of clinical
criteria.
Hand-foot-and-mouth
disease: shallow ulcers on the buccal mucosa.
DIFFERENTIAL
DIAGNOSIS
The aphthous ulcers,
herpes simplex infection, herpangina are differential diagnosis.
TREATMENT
The
supportive treatment is needed.
FOOT AND
MOUTH DISEASE
The viral
infection which rarely affect man, but does affect dogs and sheep as well as
cattle. The transmission
of disease through contact with infected animals.
CLINICAL FEATURES
Fever ,
nausea , vomiting , malaise are main clinical features.
ORAL MANIFESTATION
The
ulcerative lesion of oral mucosa. The lesion begins as small vesicle and rupture and heals within
2 weeks
MEASLES
Measles is an acute highly contagious viral disease
caused by measles virus. It is characterized by fever, URT catarrhal
inflammation, koplik’s spots and
maculopapules. The disease
may complicated with branch- pneumonia, encepholitis, hepatitis.
ETIOLOGY
Pathogen is measles virus. it has been classed as a paramyxo virus. The site of the measles
virus exists measles can be detected
from blood and nasal, pharyngeal secretions.
EPIDEMIOLOGY
The patients are
the only source of infection. The air-borne is the routes of
transmission. All age person is susceptible90% of contact people acquire the disease. The permanent immunity
acquired after disease.The winter and
spring season are main season for this viral infection.
CLINICAL
FEATURES
The incubation period
of 8-10 days. The prodromal phase
of infection is 3 to 4 days. The clinical features during prodromal phases are
fever, malaise, catarrhal inflammation of URT ,Koplik’s spots, transient prodromal rashes. The temperature rise continuously during this time
The Eruption stage
is appear 3-5 days
after fever. The rashes are maculopapular in nature.
Sequence: Behind the ear→along the hairline → face → neck → chest →
back → abdomen → limbs → hand and
feet
During Convalescent stage brown
staining , fine branny desquamation can
seen.
ORAL MANIFESTATION
Koplik's spot is a intraoral characteristic small spot, are small
irregularly shaped bluish white speck surrounded by bright red margin. It is usually
occur in buccal mucosa due to immune reaction to virus in endothelial
cells of dermal capillaries.
The palatal and pharyngeal petechiae ,generalized
inflammation, congestion
and swelling, focal
ulceration of gingiva, palate and throat are the other manifestations.
Koplik’s
spot in Measles
COMPLICATIONS
The
complications are bronchopneumonia, myocarditis, laryngitis, neurologic
complications like encephalitis, otitis media, noma.
DIFFERENTIAL
DIAGNOSIS
The rubella (German
measles) , roseola infantum , drug
rashes are the differential diagnosis.
TREATMENT
The general therapy are
rest, nursing and diet . The symptomatic
therapy for fever and cough. Then treat the complications of measles.
PREVENTION
The best method of prevention is
control the source of infection, interruption of transmissions, protection of the susceptible person. The active
immunization by MMR vaccine is best way of prevention. Passive immunization like placenta globulin or gamma globulin
mainly given for relieve symptoms.
RUBELLA
Rubella is a
mild viral illness that is produced by Toga virus. The virus is contracted
through respiratory droplets. The incubation time is from 14 to 21 days ,
and infected patients are contagious during this period. From 1 week before the
exanthem to about 5 days after the development of the rash. But infants with a
congenital rubella affected.
CLINICAL
FEATURES
Prodromal symptoms may be
seen 1 to 5 days before the exanthem
include fever, headache , malaise, anorexia, myalgia , mild
conjunctivitis , coryza, pharangitis, cough, and lymphadenopathy. The complication are arthritis , rash , encephalitis , thrombocytopenia.
The oral lesions are small discrete dark-red papules that develop on the soft
palate and may extend onto the hard palate.
TREATMENT
The Nonaspirin antipyretics and
antipruritic medications given. The passive immunity with the
administration of human rubella immunoglobulin given to relieve symptoms.
PREVENTION
The active immunization
can be done with MMR vaccine.
SMALL POX
The smallpox
is an acute viral disease, which was epidemic in nature and very fatal before the discovery of
vaccine.
CLINICAL FEATURE
The incubation period of smallpox is
7-10 days. It manifests
with high fever,nausea,vomitted,chills and headache. The skin lesions as small macules and papules appearing first on the face and then spreading rapidly to the rest of the body. The papules develop into vesicles which then
become pustules and they are small,
elevated and yellowish green with an inflamed border, which gets infected
secondarily and become hemorrhagic. The desquamation
occur when healing begins. The common complication is severe pitting or pocking
of the skin as a result of pustule formation.
ORAL MANIFESTATIONS
The ulceration of the oral mucosa and
pharynx with multiple
vesicle formation which rupture and form non specific ulcer. And the tongue is
swollen and painful making swallowing difficult.
COMPLICATION
The main complications are abscess formation with
septicemia, respiratory
infection, erysipelas,
eye infection and ear infection
MOLLUSCUM CONTAGIOSUM
It is a pox virus. It
occur on skin and mucosal surfaces. It is also consider tumour like due to the
typical localised epithelial proliferation
caused by the virus
CLINICAL FEATURES
This viral lesion is commonly seen in children and young adults. The single or multiple discrete elevated nodules occurs
on the arms, legs , trunk , face and particularly eyelids. This infection can sexually
transmitted or spread by autoinoculation. The incubation period is 14-50 days.
The lesions are hemispheric in shape with a central umblication which may be
keratinized. The oral lesion may occur on lips, tongue and buccal mucosa
HISTOLOGIC
FEATURES
Thickening and down growth
of the epithelium with the formation of large eosinophilic intracytoplasmic
inclusion bodies known as “Henderson-petterson inclusion” or “molluscus bodies”
TREATMENT
· Surgical excision
· Topical application of podophyllin or canthardin
CONDYLOMA ACUMINATUM
Condyloma
acuminta is a infectious disease caused
by Human papilloma virus.
CLINICAL
FEATURES
The condyloma
acuminta is commonly seen in children. Soft pink nodule can seen. It proliferate and
coalesce rapidly to form diffuse papillomatous clusters of varying size.
ORAL MANIFESTATION
The
nodules are small, multiple, white or pink in colour. Papillomatous,
bulbous masses scattered over tongue .
HISTOLOGIC FEATURES
The parakerotic
surface with marked underlying acanthosis. The vacuolated cells in spinous layer
can seen. Supporting
connective tissue is oedematous and dialated
capilaries and chronic inflammatory cell infiltration is common. The intranuclear
viral inclusion can be seen.
TREATMENT
The surgical
excision is main treatment. And the topical podophyllin can
be used.
CHICKENPOX
The
chickenpox is a acute viral disease caused by
varicella zoster virus. It
represent the primary infection with varicella zoster virus. It spread
through air droplets or direct contact with active lesion and portal of entry
is respiratory tract.
CLINICAL
FEATURES
The main age incidence
is between 5 – 9 years. The site predilection are face, trunk and extremities. The prodromal symptoms showssymptomatic phase of VZV
infection begin with malaise, pharangitis,
rhinitis.
The early vesicular stage is most
characteristic of the lesion,
the centrally located vesicle is surrounded by a zone of
erythema and described as “ a dew drops on a petal ”.
the centrally located vesicle is surrounded by a zone of
erythema and described as “ a dew drops on a petal ”.
The lesion occur in
successive crops over 3-4 days and lesions
in various stages are present at the same time oral lesion
precede the skin lesions.
in various stages are present at the same time oral lesion
precede the skin lesions.
COMPLICATION
The encephalitis, pneumonia, Reye’s syndrome, spontaneous
abortion or congenital defect can occur if the disease occur early pregnancy
are main complications. In immunocomprimised persons extensive cutaneous
involvement along with high fever, hepatitis, pneumonia , pancreatitis ,
encephlitis may occur.
HISTOLOGIC FEATURES
The main histologic
features are acantholysis and formation of numerous free floating tzanck cells
.
TREATMENT
The anti
viral drug like acyclovir can be used
for chickenpox.
HERPES ZOSTER
The herpes zoster, or shingles, is an acute
self-limiting viral disease of an extremly painful and incapacitating nature. It characterized
by inflammation of dorsal root ganglia.
ETIOLOGY
The etiology is reactivation of
Varicella-zoster virus. The predisposing factors for reactivation of the virus
are AIDS, leukemia,
lymphoma, other malignancies, radiation, immunosuppressive and cytotoxic drugs ,old age.
CLINICAL FEATURES
The thoracic,
cervical, trigeminal, and lumbosacral dermatomes are most commonly affected. It is characteristically, one dermatome is usually
affected. Theprodromal
symptoms are pain
and tenderness ,headache ,pulpitis , malaise, fever . After two to four days, clusters of vesicles
develop, and within two or three days evolve into pustules and ulcers, covered
by crusts . The
lesions persist for two to three weeks. The unilateral location of the lesions
is a typical pattern of herpes zoster.
Oral
manifestations occur when the second and third branches of the trigeminal nerve
are involved. Post herpetic trigeminal neuralgia is a common
complication, and rarely osteomyelitis, jawbone necrosis, and tooth loss are
seen. The diagnosis is made on the basis of clinical criteria.
DIFFERENTIAL DIAGNOSIS
Herpes simplex, erythema
multiforme are the differential diagnosis.
MUMPS
Mumps is an acute viral infection of the paramyxoviruses
family. An acute onset of
unilateral or bilateral tender, self-limited swelling of the parotid or other
salivary gland lasting more than 2 days without other apparent cause. It can lead to brain inflammation, deafness or sterility.
PATHOGENESIS
The transmission of virus is mainly respiratory
tract. Then virus can be replication in nasopharynx
and regional lymph nodes This cause viraemia 12-25 days after exposure with spread to
tissues. The multiple
tissues infected during Viraemia
COMPLICATION
The main complications are Epididymo
orchitis may lead to
atrophy, sterility, low sperm counts, pancreatitis,deafness,
arthritis, oopharitis, nephritis, myocarditis. There is a
CNS involvement in 60% cases may manifest with aseptic meningitis,encephalitis.
LABORATORY DIAGNOSIS
No Laboratory
confirmation needed typical cases. But for a typical infection needs laboratory Diagnosis. For that the virus
isolated from saliva
urine, CSF. The virus can be cculturing
in Human amnion, He la cells. The other methods are immunoflourscence
methods ELISA,
Complement fixation test
INFECTIOUS MONONUCLEOSIS
This viral infection is also called Glandular
fever. It results from exposure to
Epstein-Barr virus (EBV). The transmission
of virus through intimate contact like kissing, sharing of straws, contaminated
salivary transmission in children. The exposure during childhood is asymptomatic. But it is symptomatic
infections arise in young adults.
CLINICAL FEATURES
The glandular
fever mainly seen in children.
The main site
incidence are apart from systemic
manifestations, affects anterior and posterior cervical chain lymph nodes as
well as oropharyngeal tonsils. Intra orally lesion seen in hard palate and
gingiva.
Signs & symptoms :
The systemic signs
and symptoms are fever, lymphadenopathy
, pharangitis, rhinitis, cough, hepatosplenomegaly. In 90% cases, prominent, symmetric, tender enlargement
of anterior and posterior cervical chain lymph nodes.
ORAL
MANIFESTATION
Petechiae on hard or soft palate and enlargement of
oropharyngeal tonsils.
DIAGNOSIS
The diagnosis
is suggested by clinical presentation. The WBC count is raised with differential count
showing lymphocytosis as high as 70% - 90%. The classical serological finding –
presence of Paul – Bunnell heterophil antibody, present in 90% of affected
patients.
ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
More than 25 million cases are present in worldwide. Considered
almost 100% fatal and no known vaccine developed so far.
ROUTES OF TRANSMISSION
·
Sexual
contact
·
Infected
blood / blood products
·
Intravenous
drug abuse
·
Transplacental
transfer
PATHOGENESIS
When virus
enters the body, its DNA incorporated into primary target cell i.e. CD4+ helper
T lymphocyte. Similar
to other viral infections, antibodies to virus are formed but are not
protective.HIV virus
can remain silent or cause cell death, as a result, decrease in helper T- cells
occurs, leading to loss in immune function. There is an asymptomatic stage lasting for about
8 – 10 years after which the final symptomatic stage develops.
CLINICAL FEATURES
After inoculation, patient may be asymptomatic or develop acute response
similar to infectious mononucleosis. The acute response are fever,
generalized lymphadenopathy, sore throat, myalgia, diarrhoea, maculopapular
rash etc.
Acute syndrome clears within a few weeks and a variable asymptomatic
phase follows which may last for 8 – 10 years.
Symptomatic phase shows opportunistic infections like (pneumonia, CMV, HSV, TB etc) and neoplastic
processes like (Kaposi sarcoma, Non-Hodgkin’s lymphoma etc).
ORAL MANIFESTATIONS
GROUP 1
(LESIONS STRONGLY ASSOCIATED WITH HIV)
1.
Oral candidal infections
·
Erythematous
·
Hyperplastic
·
Pseudomembranous
2.
Hairy leukoplakia
3.
HIV associated periodontitis
·
HIV gingivitis
·
HIV periodontitis
·
Necrotizing ulcerative gingivitis
·
Necrotizing ulcerative stomatitis
4.
Kaposi sarcoma
5.
Non-Hodgkin’s lymphoma
ORAL CANDIDIASIS HIV ASSOCIATED HAIRY
LEUKOPLAKIA
PERIODONTITIS
HIV associated gingivitis Necrotizing ulcerative
gingivitis Necrotizing ulcerative
stomatitis
Stages of Kaposi sarcoma
Patch stage Plaque stage Nodular stage
GROUP 2
(LESIONS LESS COMMONLY ASSOCIATED WITH HIV):
1. Aphthous ulcers (oropharyngeal
region)
2. Idiopathic thrombocytopenia
3. Salivary gland disorders
·
Dry
mouth and decreased salivary flow
·
Uni
or bilateral swelling of major glands
4. Viral infections (apart from EBV)
·
Cytomegalovirus
· Herpes simplex virus
· Human papilloma virus
· Varicella - zoster virus
HIV ASSOCIATED APHTHOUS
ULCERS HIV ASSOCIATED HPV INFECTION HIV ASSOCIATED HERPETIC ULCERS
GROUP 3 ( LESION
SEEN IN HIV INFECTION) ;
1. Bacterial infection
· Actinomyces Israeli
· E coli
· Klebsiella pneumonia
· Cat scratch disease
2. Drug reaction
3. Lichenoid reaction
4. Epithelioid angiomatosis
5. Fungal infection other than candidiasis
·Cryptococcus neoformans
·Histoplasma capsulatum
· Aspergilus flavus
6. Neurologic disturbance
· Facial plasy
· Trigeminal neuralgia
7. Recurrent aphthous stomatitis
8.
Viral
infections
· Cytomegalo virus
· Molluscum contagiosum
DIAGNOSIS
1.
VIRAL BASED TESTS
·
Viral culture
·
PCR
·
P24 antigen detection : During window period and
late
phase of
infection
2.
ANTI-HIV ANTIBODY TESTS
·
Screening test:
ELISA is most commonly used test.
-But
it can show false positive results.
·
Western Blot test:
It is a test to detect viral antibodies.
-More accurate than ELISA.
3. IMMUNOLOGICAL
MARKERS
·
CD4+ T cell
count : Decreases
·
CD4/CD8
ratio : Reverse
4.
SALIVARY TESTS
5. GAC ELISA
TREATMENT
Highly
active Antiretro viral therapy is needed.
Three types of medications are available The initial regimens consist of two nucleoside reverse
transcriptase inhibitors and
one or two protease inhibitors. Alternatively
, two nucleoside reverse transcriptase inhibitors
and a no nucleoside reverse transcriptase inhibitor can be used.
1.
Nucleoside reverse- transcriptase inhibitors
Abacavir, didanosine, lamivudine,
stavudine, zalcitabine or zidovudine
2. Nonnuc1eoside reverse transcriptase inhibitors
Delavlrdlne, efavirenz. or nevirapine
3. Protease inhibitors
Amprenavir; indinavir; nelflnavh; ritonavir;
or saquinavir T
Reference
1.
Textbook of Oral
pathology 6th edition : Shafer
2.
Oral and maxillofacial
Pathology 2nd edition :
Neville
3.
Textbook of Oral medicine : Anil Ghom
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