HIV Infection—AIDS


HIV Infection—AIDS

The immune deficiency disease AIDS (Acquired Immunodeficiency Syndrome) is caused by the HIV virus 1, a retrovirus. It is a complex virus, whose RNA genome (8,700 bases) contains at least nine genes. The three most important of these nine are env (virus capsule protein), gag (group-specific antigen) and pol (polymerase, enzyme-coding portion in the retrovirus genome; Fig. 302).

The virus exhibits the following structural characteristics: an RNA genome at the center of which the reverse transcriptase (RT, p66 pol-gene product) is bound; gag-coded proteins determine the virion structure; the phospholipid membrane (PL) provided by the host; two env gene products; a membrane-penetrating (gp 41) glycoprotein and an externally localized glycoprotein (knobs, gp 120) anchored to it. Three genes (tat, rev, nef) have regulatory functions. The specific functions of the remaining genes have not yet been completely elucidated.

302 HI Virus The env-, gag- and pol-coded proteins (p) and glycoproteins (gp) are shown at the left, and all other structures (1–11) on the right. HIV Envelope Virus-coded 1 Knob bodies gp120 2 Transmembrane portion gp41 3 Capsule matrix p17 Host-coded 4 Phospholipid bilayer 5 MHC-proteins (receptors, p. 46) Capsid/Core 6 Capsomere proteins p24 7 RNA capsule protein p7 Genome/Enzymes 8 HIV-RNA, 2 single strands 9 RT reverse transcriptase p66 10 IN integrase p32 11 PR protease p12 HIV Genome (below) A env -coded viral surface proteins (binding sites for CD4 and membrane fusion) B gag -coded nucleocapsid and nuclear membrane C pol -coded for the enzymes RT, IN, PR and ribonucleases

HIV Disease—Epidemiology

The world wide dissemination of the HIV disease continues to increase. At the end of 2002, over 41,000,000 persons were infected with the HI virus. There are grave differences between the industrialized nations on the one hand and the developing countries on the other: While in the USA, Western Europe, Japan, Australia and New Zealand the new infections of adults have generally stabilized, the rates for the African countries south of the Sahara Desert, and in Russia continue to increase. At the present time, two thirds of all the HIV-infected adults are found in sub-Saharan Africa and Russia, and 90% of all infected children!

Unprotected heterosexual intercourse, the dissemination of uncontrolled blood products and above all the lack of prevention (information), as well as the enormous costs of treatment may be responsible for the current situation. Even more perplexing is the fact that the HI virus appears in various types and subtypes (Reichart & Gelderblom 1998, Reichart & Philipsen 1999), which makes efforts toward treatment or even immunization infinitely more complex.

The battle against the AIDS pandemic must also be waged against the socioeconomic backdrop.

Ninety percent of all HIV-infected individuals world wide live in developing countries, but 90% of all monies spent for information, prevention and treatment are expended in the industrialized countries–ca. $10,000 per infected person per year.

Epidemiologic research has shown that we must differentiate not only between countries and their various stages of economic development. Even within the industrialized nations, there are clear differences between persons of different socioeconomic classes. For example, in the USA the infection rate for Blacks is almost five times higher than for white males. The difference between Afro-American and Caucasian females in the USA is even more dramatic (Fig. 304, right).

Because it is extremely unlikely that the differences between industrialized and developing nations, as well as between different socioeconomic standards will ever be reconciled, the highest priority must be given to the development of effective and inexpensive medicines, and above all an effective vaccine (Mann and Tarantola 1998).

303 World Wide Distribution of HIV-infected Individuals, 1997 By far the majority of HIV-infected person live in sub-Saharan Africa (20,800,000), as well as in south and southeast Asia (6,000,000), followed by Latin America (1,800,000). Various HIV subtypes (A–G) can be differentiated. Type B predominates (80%) in Europe and North America. By the end of 2002, over 41,000,000 persons world wide were infected with HIV.
304 Increase in HIV-infected Adults, 1980–1998 Left: In the industrialized countries, the number of infected adults has decreased somewhat, following the initial increase. South of the Sahara Desert–but also in south and southeast Asia–a dramatic increase occurred. Right: New infections per 100,000 adults and adolescents in the USA, 1996; the numbers are higher in individuals in lower socioeconomic groups.

Classification and Clinical Course of HIV Disease

With ever-increasing knowledge, the classification of the HIV disease has already been modified many times, and additional variations will surely be implemented in the future. The classification derives from data from the USA Centers for Disease Control and Prevention (CDCP). This classification is based on the number of CD4 cells (stages 1–3) in relation to clinical symptoms (stages A–C) (Fig. 305).

Besides this classification, today the most significant parameter of the clinical course of disease is the number of free virus copies per milliliter of blood plasma, the so-called “viral load.” This is determined using the polymerase chain reaction (PCR).

HIV disease develops very rapidly following the initial infection. Billions of HIV particles destroy millions of CD4 lymphocytes. This bitter “war of attrition” between HI viruses and host cells goes on continually for years. During the further (average) course of the disease–about 6 months after infection–the number of freely circulating viruses decreases dramatically and the number of immune cells again increases. A balance between attack and defense can remain constant for ca. 10 years, until the number of viruses again increases dramatically and the host defense breaks down (Fig. 306).

Even from patient to patient, the disease can assume extra-ordinarily different clinical courses. “Long survivors” are those individuals who live longer than 10 years after infection, while others with the disease have only a short postinfection life span. A prognosis concerning the course of the disease is possible by measuring the viral load. Mellors (1998) measured the viral load in 1,600 untreated HIV-infected males, and reported that 70% of his study population who exhibited more than 30,000 virus copies per milliliter of blood plasma died within six years (mean lifespan: 4.4 years). In contrast, less than 1% of the untreated patients died within six years if their viral load was below 500 copies/ml. In the latter group, the mean life expectancy was more than 10 years.

It is now clear that the determination of viral load provides important information concerning prognosis and therapy. Using today’s anti-retroviral medicinal polytherapy (p. 149), the number of virus particles can be held below the level of detection.

305 CDCP Classification Close scrutiny of the CDCP classification clearly reveals that patients with a relatively high number of CD4 cells may already exhibit AIDS symptoms (C2), while, on the other hand, infected individuals with only low levels of CD4-cells may remain asymptomatic (A2).
306 “Average” Clinical Course of HIV Disease Immediately following HIV infection, there follows a ca. 6-month acute phase (bouts of fever, lymphadenitis etc), followed by a years-long asymptomatic period. This is characterized by a low viral load and a positive immune response (T-helper and T-killer cells, antibodies etc.). On average, 8–12 years later, the viral load increases and host defense collapses. The “average” clinical course depicted here varies significantly from patient to patient.

Oral Manifestations of HIV Disease

In addition to numerous somatic symptoms, the HIV disease can also be characterized by pronounced oral manifestations. The progress in systemic medical therapy has fortunately reduced many oral symptoms, e.g., bacterial and fungal infections, viral infections, neoplasms and other pathology of unknown etiology (Fig. 307).

The oral lesions are often painful and can compromise the patient’s quality of life. The time of appearance of oral manifestations will be determined by the CD4 cell count and the viral load (Fig. 308). Occasionally, however, oral alterations—especially linear gingival erythema (LGE) and necrotizing periodontitis (NUP)—occur at unpredictable times during the course of the HIV disease.

The dentist must be fully aware of the oral manifestations of HIV disease; in numerous cases, a dentist has diagnosed oral alterations that lead to suspicion of HIV infection, only to have those suspicions subsequently corroborated after medical examination by the physician.

307 Some Oral Manifestations of HIV Disease Most of the alterations (listed to the right) can be diagnosed by the dentist. LGE, NUG and NUP can only be treated in the dental practice (p. 151). All other disease manifestations must be treated in collaboration with the physician.
308 Occurrence of Disease in Correlation with the CD4 Cell Number (“Marker” Diseases) While candidiasis can occur relatively early, the severe systemic diseases such as Pneumocystis carinii pneumonia (PcP), Toxoplasmosis, infections with intracellular Mycobacterium avium (MAI), Cytomegalovirus (CMV) pneumonia etc. occur only when the CD4 cell count drops.
309 Association Between Certain Oral Symptoms and HIV Disease The frequency of occurrence of these opportunistic diseases is also dependent on the stage of the HIV disease (Weinert et al. 1996).

Bacterial Infections in HIV

  • Linear gingival erythema (LGE)

  • Necrotizing gingivitis/periodontitis (NUG/NUP)

The disease states marked with a solid bullet (•) on this page and the pages that follow are depicted and described.

LGE is clearly differentiable from simple plaque-elicited gingivitis. It is characterized by a clearly demarcated band of reddening in the marginal gingiva. Classic periodontitis—both “chronic” and “aggressive” forms—do not occur in HIV-disease patients any more frequently than in other individuals; on the other hand, NUP occurs much more frequently, often exhibiting an extremely rapid clinical course of attachment loss.

Th significance of certain microorganisms in the etiology of LGE and NUP remains unclear. One finds periodontopathic microorganisms as seen in aggressive forms of periodontitis (p. 96), but often also significant increases in Candida albicans (Ca). The spotty erythema on the attached gingiva, and the frequent observation of this fungus in niches and pockets can be attributed to Ca. In those not responding to mechanical therapy, the cytomegalovirus is often detected.

310 Linear Gingival Erythema (LGE) Note the even band of erythema along the gingival margin and papillae. It is unclear whether such LGE (in the absence of treatment) can develop into NUP. The latter appears to be much more closely associated with ulcerative gingivitis (Fig. 311). Treatment consists of mechanical cleaning with betadine irrigation, motivation to improve oral hygiene and, in severe cases, CHX rinses. Courtesy J. Winkler
311 Ulcerative Gingivitis—NUP, Initial Stage 23-year-old female drug addict. The inflammation and ulcerations are similar to those observed in classic ulcerative gingivoperiodontitis. In the absence of treatment, the destruction of gingival tissue can progress rapidly. Left: Severe, painful, ulcerative gingivitis in a 28-year-old female drug addict. The case was treated successfully (Figs. 329335); she returns for regular recall and is recurrence-free for 7 years.
312 Very Advanced NUP 45-year-old homosexual male with extremely severe and painful NUP. Exposed bone could be probed in the interdental areas. In such severe cases, osseous sequesters may form. This patient was in the end stage of AIDS, and died 3 months later. The standard NUP therapy used here is described on pages 151–154.

Fungal Infections

  • Candidiasis

    • Atrophic/Erythematous

    • Angular cheilitis

    • Pseudomembranous

    • Hyperplastic

      • Histoplasmosis

The most common and earliest appearing fungal infection in HIV disease is candidiasis in its many and varied forms. Approximately 95% of all fungal diseases are caused by Candida albicans; other fungi have only minor medical significance. Candida albicans is also found in a high percentage of healthy individuals, without causing any clinical symptoms. If host defense mechanisms are reduced, as is the case in HIV disease, proliferation of the fungi can occur by growth of hyphae and the formation of mycelia. The latter can invade the mucosa and lead to clinical manifestations of the types listed above. Oral Candida infections have a tendency to recur. Spread into the respiratory tract or the gastrointestinal tract is an indication of progression of the HIV disease, and is a complication to be taken very seriously by the patient and the physician.

313 Pseudomembranous Candidiasis The whitish, painless layer on the gingiva and mucosa of this 27-year-old drug-addicted HIV patient can be easily wiped away. Treatment for cases limited to the oral cavity generally consists of careful removal of the pseudomembrane, and in severe cases systemic antimycotics. Right: Candida mycelia in culture.
314 Atrophic, Erythematous Candidiasis This 45-year-old, HIV-infected homosexual male exhibits reddish lesions in the middle of the palate. Similar alterations can also be observed on the edentulous alveolar ridge, attached gingiva and the dorsum of the tongue. The lesions may be painful. Medicinal treatment involves topical rinsing with CHX, and systemic administration of the antimycotic Diflucan (Fluconazol).
315 Angular Cheilitis (Perlèche) Typical fissures at the corner of the mouth in a 32-year-old heterosexual, HIV-positive patient (promiscuity). These lesions are very painful and render dental treatment difficult. There is an association between Candida albicans and Streptococcus aureus. Perlèche is also observed in immunodeficient elderly individuals, as well as patients with severe overbite. The treatment consists of topical antimycotic agents (see above).
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Jul 2, 2020 | Posted by in Dental Hygiene | Comments Off on HIV Infection—AIDS
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