HUMAN IMMUNODEFICIENCY

VIRUS AND ACQUIRED

IMMUNODEFICIENCY
SYNDROME (HIV/AIDS)

Rezky Fauziah P. Saly Salim Alatas Wempi Gigih

Fristiantama
1406570480 1406572523 1406579214
PEMICU
 Pasien pria usia 34 tahun datang dengan keluhan sariawan
di rongga mulut dan bibir yang melepuh. Pada
pemeriksaan fisik, pasien tampak lemah dan kurus serta
pasien mengatakan bahwa kulitnya menghitam. Pasien
sedang menjalani rehabilitasi penggunaan Narkoba. Pasien
mengatakan bahwa dirinya HIV positif dan sudah diberi
obat antiretroviral namun pasien kadang tidak minum obat
karena pasien merasa obatnya membuat mual dan muntah.
 Pada pemeriksaan rongga mulut, terdapat ulser multipel
berukuran 5-10 mm di mukosa bukal dan palatum. Bibir
pasien tampak kering, terdapat erosi, dan krusta merah
kehitaman. Pasien mengatakan kondisinya muncul sejak 3
hari yang lalu.
DEFINITION
 HIV is a lymphotrophic virus that belongs to the family
retroviridae and subfamily lentivirus (include HIV-1 and
HIV-2) that causes HIV infection and over time acquired
immunodeficiency syndrome (AIDS)
 AIDS is a disorders characterized by a profound cell-
mediated immunodeficiency consequential to
irreversible suppression of T lymphocytes by the HIV
thus creating a condition failure of the immune system
allows life-threatening opportunistic infections,
malignancies and autoimmune disorders
 The entire spectrum of the infection is often referred to
as HIV/AIDS. (rubin)
EPIDEMIOLOGY
 HIV is a descendant of a specific simian
immunodeficiency virus (SIV)
 SIVcpz is a immediate precsuor to HIV-1 which natural
host is the chimpanzee of the subspecies Pan troglodytes
troglodytes
 SIVsm is a immediate precursor to HIV-2 which natural
host is the sooty mangabey
 Both HIV-1 and 2 have the same modes of transmission,
and both may cause immunosuppression and AIDS.
 Approximately 35.2 million persons were living with
HIV at the end of 2012
 Rates of new HIV infection continues to decline in many
countries and populations, and for much of the world
(the largest declines in the Caribbean and in sub-Saharan
Africa) HIV pandemic has passed peak incidence
PATHOGENESIS
 HIV-1 is an enveloped member of the retrovirus family,
belonging to the subfamily of lentiviruses
 Mononuclear phagocytes and CD4 helper T lymphocytes
are the main targets for HIV-1 infection, although the
virus can enter other cells, such as B lymphocytes,
astrocytes, endothelial cells and intestinal epithelium
PATHOGENEIS
 HIV enters the host
 Envelope of virus binds to the CD4 molecule on
dendritic cells
 Cell entry requires a coreceptor

 Infected cells fuse with CD4+ (helper) T Lymphocytes

and spread to the deeper tissues
 Depletion of T lymphocites population

 Impaired immune function and dysregulation

MOLECULAR PATHOGENESIS
The replicative cycle of HIV-1
1. Binding
2. Internalization
3. DNA synthesis
4. Integration
5. Replication
6. Dissemination
DISEASE PROGRESSION
 Upon initial or acute infection usually has minimal
symptoms (40% - 90% characterized by varying degrees
of fever, fatigue, maculopapular rash, headache,
lymphadenopathy, pharyngitis, myalgia, arthralgia, GI
distress, night sweats, and oral or genital ulcers) 
approximately 10 to 12 years in the absence of
antiretroviral therapy (clinical latency)
 Factors such as age or genetic differences among
individuals, the level of virulence of an individual strain
of virus, and co-infection with other microbes may
influence the rate and severity of disease progression
TRANSMISSION
 The prime modes of transmission for HIV continue to be
:
1. Unprotected penetrative sex between men
2. Unprotected heterosexual intercourse
3. Injection drug use
4. Unsanitary injections and blood transfusions
5. Mother to child spread during pregnancy, delivery, or
breast feeding
 More than 80% of adults infected with HIV are infected
through the exposure of mucosal surfaces (linings of the
vagina, vulva, rectum, penis, or the oral cavity) to the
virus. 20% are infected by percutaneous or intravenous
inoculations
 Breaks in the mucosal barrier and the presence of
increased inflammation due to genital ulcer disease,
urethritis, or cervicitis increase the risk of acquiring HIV
infection
RISK FACTORS
 Behaviours and conditions that put individuals at greater risk
of contracting HIV include:
 Having unprotected anal or vaginal sex;

 having another sexually transmitted infection such as

syphilis, herpes, chlamydia, gonorrhoea, and bacterial
vaginosis;
 Sharing contaminated needles, syringes and other injecting
equipment and drug solutions when injecting drugs;
 Receiving unsafe injections, blood transfusions, tissue
transplantation, medical procedures that involve unsterile
cutting or piercing; and
 Experiencing accidental needle stick injuries, including
among health workers.
CLINICAL
FEATURES AND
SYMPTOMS
  HIV may cause an initial glandular-fever-like illness but
may be asymptomatic.
 Infections with viruses, fungi and mycobacteria
supervene, and patients may develop virally related
neoplasms such as Kaposi's sarcoma, lymphoma and
cervical or anal carcinoma.
 The patient develops opportunistic infections (from
commensal organisms such as Candida), and may
contract exogenous pathogens (such as TB)

Scully C. Handbook of Oral Disease. Diagnosis and Management. 2nd ed. London: Martin Dunitz Ltd; 2001.
Scully C. Handbook of Oral Disease. Diagnosis and Management. 2nd ed. London: Martin Dunitz Ltd; 2001.
Scully C. Handbook of Oral Disease. Diagnosis and Management. 2nd ed. London: Martin Dunitz Ltd; 2001.
Scully C. Handbook of Oral Disease. Diagnosis and Management. 2nd ed. London: Martin Dunitz Ltd; 2001.
Scully C. Handbook of Oral Disease. Diagnosis and Management. 2nd ed. London: Martin Dunitz Ltd; 2001.
Cawson RA, Binnie WH, Barrett AW, Wright JM. Oral Diseases. 3rd ed. Saint Louis: Mosby; 2001.
FARMAKOTERAP
I
 ARV DRUG CLASSES

 Currently available antiretroviral drugs belong to two

major classes:
 i)  Reverse Transcriptase Inhibitors (RTIs)
 ii)  Protease Inhibitors (PIs)

 Reverse transcriptase Inhibitors are further divided into 3

groups:
 i)  Nucleoside Reverse Transcriptase Inhibitors (NsRTIs)
 ii)  Nucleotide Reverse Transcriptase Inhibitors (NtRTIs)
 iii)  Non-nucleoside Reverse Transcriptase Inhibitors
(NNRTIs)

Source:https://www.who.int/hiv/ARV-guidelines.pdf
 ANTIRETROVIRAL DRUGS IN EACH OF THE CLASSES

• A combination of two drugs is

recommended for the treatment of HIV
infection.
• The choice of drugs is based on the patient
current drug resistances (if any),
accompanying illnesses, and personal
circumstances

Source:https://www.who.int/hiv/ARV-guidelines.pdf
 STANDARD ANTIRETROVIRAL DRUG DOSES

Source:https://www.who.int/hiv/ARV-guidelines.pdf
 STANDARD ANTIRETROVIRAL DRUG DOSES

Source:https://www.who.int/hiv/ARV-guidelines.pdf
DRUG SPECIFIC SIDE EFFECTS

Source:https://www.who.int/hiv/ARV-guidelines.pdf
POST-EXPOSURE
PROPHYLAXIS
  Post-exposure prophylaxis, or PEP, is another name for
emergency HIV treatment.
 PEP is not a cure for HIV, it is a form of HIV prevention.

 It is a short course of antiretroviral drugs that stops

exposure to HIV from becoming a life-long infection.

https://www.cdc.gov/hiv/basics/pep.html
 USUALLY YOU SHOULD ONLY TAKE PEP IF...

a it has not been longer than 72 hours since exposure to

HIV
a you are not already living with HIV
aa mucous membrane (including: eyes, mouth, vagina,
rectum) has had direct contact with someone’s bodily uid
that might be infectious
a an open wound has had direct contact with someone’s
bodily uid that might be infectious
athe source of exposure is infected
with HIV or their HIV status is unknown

https://www.cdc.gov/hiv/basics/pep.html
 PEP AND HIV TESTING
 Not everyone is given PEP, and it is not available everywhere.
 A healthcare professional will advise you if they think you
should take PEP.
Do not assume you will be offered it.
 If you took PEP - get tested 3 and 6 months after potential
exposure.
 If you didn’t take PEP - get tested 3 months after potential
exposure.
 may cause side effects like nausea in some people. These side
effects can be treated and aren’t life-threatening.

https://www.cdc.gov/hiv/basics/pep.html
Source: https://www.cdc.gov/hiv/basics/pep.html
ORAL
MANIFESTATION
IN HIV/AIDS
PATIENTS
ORAL MANIFESTATION IN HIV/AIDS
PATIENTS
 Oral features of HIV/AIDS reflect the T-cell
immune defect  consequence of fungal or viral
or sometimes mycobacterial or parasitic
infections
 Oral lesions may:
 indicate HIV infection that is previously
undiagnosed
 be used in staging and therapy decisions
 cause the patient pain or aesthetic problems
 increase the liability for HIV transmission.
CLASSIFICATION BY THE EC
CLEARINGHOUSE
CANDIDIASIS
 Most common intraoral manifestation of HIV
 First found during the early symptomatic stage of
infection  AIDS will develop within 2 years in
untreated patients.
 Clinical features: Thrush (pseudomembranous
candidiasis), erythematous (palate and dorsum of the
tongue), cheilitis, hyperplastic candidiasis.
 Site: hard palate, tongue and soft palate.
 Diagnosed by its clinical appearance and by
detection of organisms on smears using potassium
hydroxide (KOH), PAS, or Gram's stain.
 Treatment:
 Nystatin: ineffective.
 Topical clotrimazole: treatment of choice, has high rate of
recurrence.
 Systemic azole: given when patient is not receiving
effective retroviral therapy and CD4+ count below 50%, has
high drug interaction risk.
 If azoles fail, then IV amphotericin B can be administered.
ORAL HAIRY LEUKOPLAKIA
 Occurs in about 20% of persons with asymptomatic HIV
infection
 Hairy leukoplakia is almost always a manifestation of HIV
infection  clinicians should arrange evaluation of HIV
disease.
 Site: lateral border of the tongue, but has been found on the
buccal mucosa, soft palate, and pharynx.
 Associated with EBV infection

 Diagnosis: can be made by clinical appearance or with

biopsy for definitive diagnosis
 Treatment : not often required, resolves with aciclovir (2.5
to 3 mg per day for 2 to 3 weeks) or antiretroviral agents.
HIV-ASSOCIATED PERIODONTAL
DISEASE
 Include Linear Gingival Erythema (LGE),
Necrotizing Ulcerative Gingivitis and Periodontitis
(NUG and NUP), Necrotizing Stomatitis (NS) 
Unknown relationship between these conditions and the
progression of HIV disease.
 It occurs disproportionately to the level of oral hygiene
and plaque control.
 The presenting clinical features of these diseases often
differ from those in non-HIV-infected persons.
CLINICAL APPEARANCE
 Differential diagnosis: complaints of severe pain, rapid
onset, and rapid destruction in an often extremely
clean mouth
 Therapy  plaque removal, local debridement,
irrigation with povidone-iodine, scaling and root
planing, and maintenance (chlorhexidine mouth rinse 1-
2x daily)
 LGE  If persists, systemic antifungal medications is
needed
 NUP  metronidazole (one 250-mg tablet four times
daily), amoxicillin/clavulanate (Augmentin)(one 250-
mg tablet three times daily), or clindamycin (one 300-
mg tablet three times daily)
KAPOSI SARCOMA
 Common neoplasm in AIDS.
 Etiology: Human herpesvirus 8 (HHV8)

 Intraoral lesions may be the first manifestation of late-

stage HIV disease (AIDS).  used in diagnostic of
AIDS
 May occur intraorally, either alone or in association
with skin and disseminated lesions.
 Oral KS frequently involves the palate, the attached
gingiva and the dorsum of the tongue and oropharynx.
 HIV-associated Kaposi sarcoma is more aggressive than
others and usually produces multiple lesions (the face
and trunk).
CLINICAL
APPEARANCE

• Early lesion:
asymptomatic
macule 
progresses to
papule, nodule,
ulcer and painful
• May enlarge,
ulcerate, and become
infected Good oral
hygiene is essential
 KS must be distinguished from vascular lesions (hematomas,
hemangiomas) and pigmented lesions (oral melanotic macules)
 Diagnostic test: histologic examination (early lesions may be
difficult to diagnose histologically  they resemble
endothelial proliferation)
 Treatment is determined on the basis of the number, size, and
location of the oral KS lesions. 
 Treatment:
 Surgical
 Localized intralesional chemotherapy with vinblastine
 Systemic chemotherapy.
NON-HODGKIN LYMPHOMA (NHL)
 AIDS-related lymphomas can develop in intraoral sites or
salivary glands far more frequently than in HIV-negative
persons.
 Site: the palate or gingiva

 The tumours form soft painless swellings which ulcerate

when traumatised.
 Associated with Epstein-Barr Virus (NHL) or Karposi
Sarcoma-associated Herpes Virus (plasmablastic
lymphomas)
 Treatment usually involves a combination of chemotherapy
and radiation.
 Prognosis is very poor, with death occurring within months
of the diagnosis
HERPES SIMPLEX VIRUS (HSV)
INFECTION
 In HIV-infected patients, the lesions are more severe,
occur in an atypical pattern, and may persist for
months.
 Chronic ulcers often on keratinized mucosa and/or
vermillion borders of lips and perioral skin
 Diagnosis by: Clinical plus investigations; cytology,
electron microscopy, DNA studies or biopsy
 Treatment: Systemic acyclovir, valacyclovir, or
famciclovir for minimum 5 days and an elixir or syrup of
diphenhydramine (Benadryl) of 12.5 mg/5 mL  pain
control.
VARICELLA ZOSTER
 Zoster typically begins with local pain and discomfort, and
then progresses to a localized or segmented erythematous,
maculopapular eruption along a single dermatome.
 Blisters and crusts usually last 2-3 weeks, and necrotic lesions
may last for up to 6 weeks  significant scarring.
 Patients with advanced HIV infection may present with
prolonged lesion formation, progressive local extension,
and viral dissemination
 In immunocompromised hosts, zoster lesions may be
particularly bullous, hemorrhagic, necrotic, and painful.
 Recurrent VZV infection is common in HIV-infected patients,
but the course is more severe  lead to complication such as
pain (post herpetic neuralgia) and in intraoral (periodontitis,
tooth exfoliation, and osteonecrosis of the jaw.)
 The majority of HIV-infected patients with zoster do not
develop life-threatening complications, and most patients
have an uncomplicated clinical course
 Treatment: Valacyclovir 1 g PO tid; famciclovir 500 mg PO
tid; acyclovir 800 mg PO 5 times per day. Intravenous
acyclovir may be needed for severe herpes zoster in patients
with immunosuppression.
HUMAN PAPILLOMAVIRUS
 The risk of infection by high oncogenic types of HPV is
13 times greater in HIV positive individuals who practiced
oral sex with more than one person during the previous
year.
 Lesions usually are multiple and may be found on any oral
mucosal site.
 Papillomaviruses have been isolated from proliferative
lesions, such as verruca vulgaris, condyloma acuminatum
and focal epithelial hyperplasia.
 Treatment of choice is surgical removal of the lesion(s).
Other treatment modalities include topical podophyllin,
interferon, and cryosurgery.
PERSISTENT GENERALIZED
LYMPHADENOPATHY
 An early sign of HIV infection, found in about 70% of
infected patients during the latent stage of infection.
 Must be present longer than 3 months and in two or
more extrainguinal locations.
 Anterior and posterior cervical, submandibular, occipital,
and axillary nodes are most frequently involved.
 The nodes tend to be larger than 1 cm in diameter
DIAGNOSIS
APTHOUS STOMATITIS
 The cause of these ulcers is unknown  probably stress
and unidentified infectious agents.
 In HIV-infected patients, the ulcers are well
circumscribed with erythematous margins.
 About 66% of lesions are of the more uncommon forms
—major (2-4 cm in size, painful, persist) and
herpetiform (cluster of small ulcers)
 Lesions that are chronic or atypical, or that do not
respond to treatment, should be biopsied.
 Difficult to diagnose because its resemblances to another oral
lesion.
 Treatment: potent topical or intralesional corticosteroids.

 Systemic steroids generally are avoided, to prevent further

immunosuppression.
 Fluocinonide (0.05%) ointment mixed with equal parts Orabase
applied six times daily OR clobetasol (0.05%) ointment mixed with
equal parts Orabase applied three times per day
 Multiple ulcers and unreachable area  Dexamethasone elixir (0.5
mg/5 ml) used as a mouth rinse and then expectorated, 2-3x/day
 For HIV-infected persons with oral and gastrointestinal aphthous-like
ulcers  systemic steroid therapy (prednisone 40 to 60 mg/day for 7
to 10 days)
 Thalidomide treatment has yielded good response but should be
used for only a short time, because the drug can enhance HIV
replication.
HIV-ASSOCIATED SALIVARY CONDITION
 Found in 5% of HIV-infected patients and can occur any time during the infection
(mostly in early stage)
 Symptoms  Parotid enlargement (unilateral or bilateral), asymptomatic,
decreased salivary flow (xerostomia or dry mouth).
 Associated factors: sex, stage of HIV infection, risk group of HIV infection,
systemic disease, and medication use.
 Risk is increased for cysts (Benign Lymphoepithelial Cyst) of the parotid (usually
present as painless bilateral parotid enlargement) and lymphoma.
 Assesment: thorough history related to the time of onset and rate of growth as well
as symptoms associated with the mass such as pain and discomfort. 
 The diagnosis of BLEC is very specific to HIV infection  mandatory to perform
an HIV test as part of the diagnostic work- up
 Treatment: antiretroviral therapy, radiation, surgery. Associated xerostomia can be
managed with sialogogues and saliva substitutes.
HISTOPLASMOSIS
 Histoplasmosis is the most common endemic
respiratory fungal infection in the United States and
usually is subclinical and self-limiting.
 Dissemination of infection occurs in about 5% of
patients with AIDS who live in areas in the United States
where the fungus is endemic.
 The treatment of choice for disseminated histoplasmosis
is intravenous amphotericin B.
 Oral itraconazole also has been found to be effective
and has fewer adverse effects, with better patient
compliance.
THROMBOCYTOPENIA PURPURA
 Thrombocytopenia is found in about 10% of HIV-infected patients
in any stage of the disease.
 Skin manifestations are most common, but petechiae, ecchymosis,
and spontaneous gingival bleeding can occur in the oral cavity.
 Platelet counts below 50,000/mm3 may result in significant
bleeding with minor surgical procedures  Platelet replacement
may be indicated
 Examination of the marrow to check the presence of lymphoma or
opportunistic infections (fungi or mycobacteria). 
 Treatment should be reserved for patients with clinically significant
symptoms such as recurrent epistaxis, gingival or subconjunctival
bleeding, or gastrointestinal hemorrhage. 
HYPERPIGMENTATION
 Melanin pigmentation has been reported to occur in HIV-
infected patients. Several of the medications
(ketoconazole, clofazimine, and zidovudine) used to treat
these patients may cause melanin pigmentation.
 In dark-skinned persons (Hispanics and blacks),
treatment with AZT may result in hyperpigmentation of
the nails, oral mucosa, and skin.
 Addison-like pigmentation also may occur because of
destruction of the adrenal gland.
 HIV infection itself may cause melanin pigmentation.

 Treatment: not indicated. Single lesions may have to be

biopsied so that melanoma can be ruled out.
REFERENSI :
 Essential microbiology for dentistry 4th edition. Lakshman
Samaranayake
 Burkets Oral Medicine 12th edition. Michael Glick

 Rubin’s Pathology. 6th edition. Raphael Rubin

 https://www.who.int/news-room/fact-sheets/detail/hiv-ids

 https://www.who.int/news-room/fact-sheets/detail/hiv-aids

 Scully C. Handbook of Oral Disease. Diagnosis and Management.

2nd ed. London: Martin Dunitz Ltd; 2001.
 Cawson RA, Binnie WH, Barrett AW, Wright JM. Oral Diseases. 3rd
ed. Saint Louis: Mosby; 2001.
 https://www.cdc.gov/hiv/basics/pep.html diakses pada 23 Maret 2019

 https://www.who.int/hiv/ARV-guidelines.pdf diakses pada 23 Maret

2019
 PERTANYAAN
 Nabila: lesi oral bisa muncul kapan? Apakah bisa dicegah?
Apakah lesi oral pada pasien stage lanjut masih bisa dirawat?
 Berdasarkan clinical staging untuk HIV/AIDS berdasarkan WHO,
lesi oral bisa muncul sejak stage 2, dimana umumnya pasien
sudah ada gejala namun tergolong mild. Lesi oral yang muncul di
stage ini biasanya berupa herpes zoster, angular cheilitis, dan
recurrent oral ulcerations

https://www.who.int/hiv/pub/guidelines/clinicalstaging.pdf
 Nadia: tindak lanjut jika menemukan pasien susp HIV
bagaimana?
 Pasien bisa dirujuk untuk melakukan tes HIV. Sistem untuk
melakukan tes HIV bisa berupa voluntary counselling and
testing (VCT) atau provider-initiated counselling and testing
(PICT). Pastikan pasien telah setuju dan mau untuk
melakukan tes sebelum dirujuk. Pasien juga di KIE dan
berikan konseling agar pasien tidak stres.
 Tsany: apakah drg
bisa mengajukan tes
HIV ke pasien susp
HIV? Tes yang
diperlukan untuk HIV
apakah cukup elisa
saja?
 Bisa. Screening awal
bisa menggunakan
rapid test atau dengan
ELISA. Berikut
adalah algoritma
untuk diagnosis
HIV/AIDS
 Ola: apakah bisa PEP dilakukan dengan kondisi post-
exposure lebih dari 72 jam?
 PEP tidak di rekomendasi dilakukan jika waktu sejak
pemaparan sudah lebih dari 72 jam dikarenakan virus HIV
membutuhkan waktu 72 jam untuk berikatan ke CD4+ sehingga
lebih dari itu, diperkirakan virus sudah berhasil menginfeksi.
 Reny: bagaimana pengobatan pasien2 hiv dimana
rekurensi tinggi? Obat2 anti retroviral diberikan stage
kapan?
 Umumnya, jika pasien telah dalam perawatan ART, maka
kemungkinan munculnya gejala, terutama lesi oral, akan
menurun karena manifestasi / gejala seperti lesi oral hanya
muncul jika ada gangguan imunitas sehingga diharapkan jika
pasien sudah melakukan pengobatan ART, kemungkinan
terjadinya manifestasi terutama oral menurun. Obat ART
diberikan sedini mungkin setelah diagnosis definitf didapatkan
 Adit: manifestasi oral meningkatkan resiko transmisi
HIV, maksudnya apa?
 Dikarenakan hampir lebih dari 80% orang dewasa dengan
HIV terinfeksi melalui permukaan mukosa (temasuk rongga
mulut) maka jika ada lesi oral yang mengakibatkan kerusakan
permukaan mukosa dan inflamasi, maka transmisi HIV akan
lebih mudah dan penderita pun memiliki resiko yang lebih
besar untuk tertular HIV
 Vira: treatment OHL pada pasien HIV
 Oral hairy leukoplakia umumnya akan sembuh sendiri dalam
jangka waktu 1-2 minggu dan asimptomatik. Namun, jika
pasien memiliki keluhan nyeri atau estetik, maka bisa
diberikan valacylovir atau agen topikal seperti podophylin
resin dicampur krim acyclovir. Pasien juga diinstruksikan
untuk menyikat lidah dengan sikat gigi atau tongue scraper
 Isni: sebelum PEP, apakah perlu dilakukan tes HIV dulu atau
langsung? Apakah ada obat antiretroviral diberikan?
 Tes HIV tidak perlu diberikan sebelum PEP karena tes dilakukan dengan
mendeteksi antigen p24 HIV dan antibodi HIV-1/2. Seroconversion adalah
waktu dimana antibodi telah bisa dideteksi sehingga jika seseorang terkena
virus dan melakukan tes sebelum seroconversion dimulai, hasilnya akan
negatif. Umumnya, antibodi baru bisa terdeteksi dalam waktu 3-12
minggu sehingga sebaiknya tes dilakukan 2x yaitu sejak dini (minggu 3-4
setelah terpapar) dan evaluasi (minggu 12 setelah terpapar).
TAMBAHAN:
CDC STAGING OF HIV INFECTION

Sumber: https://www.cdc.gov/hiv/statistics/surveillance/terms.html
CDC STAGING OF HIV INFECTION
 HIV infection diklasifikasikan pada stage 3 (AIDS)
ketika sistem imun seseorang yangv terinfeksi HIV
menjadi severly compromised (berdasarkan perhitungan
jumlah CD4) dan menjadi sakit karena infeksi
oportunistiknya.
 tanpa perawatan, AIDS berkembang biasanya 8 sampai
10 tahun sejak infeksi pertama, tetapi dengan diagnosis
dan perawatan dini, dapat berkembang jauh lebih lambat
beberapa tahun.

Sumber: https://www.cdc.gov/hiv/statistics/surveillance/terms.html
Scully C. Handbook of Oral Disease. Diagnosis and Management. 2nd ed. London: Martin Dunitz Ltd; 2001.