Introduction

– Jürgen Kurt Rockstroh –

Acquired Immune Deficiency Syndrome (AIDS) was first described as a new clinical entity in 1981. Initial reports were based on an unusual increase in the incidence of Kaposi sarcoma (KS) and Pneumocystis pneumonia (PCP), diseases that were considered at that time to occur rarely. While both diseases are occasionally observed in different populations (e.g., KS in older men from the Mediterranean region or PCP in patients with leukemia after intensive chemotherapy), the occurrence of these diseases as indicators for severe immunodeficiency had not been observed before in otherwise healthy young individuals. Because the initially affected population were men who had sex with men (MSM) the disease as well as those with the disease were highly stigmatized. Though initially lifestyle and behavioral factors were hypothesized to be causally related, finally in 1983 the human immunodeficiency virus (HIV) was identified as the true cause of AIDS.

In 1987 the first antiretroviral agent, AZT (zidovudine, Retrovir®) was licensed for the treatment of HIV. Despite the failure of this therapeutic concept in terms of monotherapy in achieving long-term suppression of HIV replication, symptoms and clinical manifestations of HIV infection were temporarily relieved with AZT (at 1500 mg/day) and the occurrence of AIDS was slightly delayed. What happened next is unprecedented in medicine to date – within a few years of its discovery an inevitably deadly disease turned into a disease with durable and effective treatment options. The rapid introduction of additional antiretroviral drug classes and the concept of highly active antiretroviral therapy (HAART, an acronym that will be replaced in this book by ART) enabled a durable suppression of viral replication thereby preventing disease progression – as long as the antiretroviral drugs were tolerated and regularly taken. Long-term toxicities and the emergence of resistance led to a search for and identification of further promising drugs with other therapeutic mechanisms of action or better resistance profiles. In parallel, administration modalities and tolerability of antiretroviral drug regimens improved significantly. In 2010 several HIV therapies are available that only require an intake of 1–3 tablets a day mostly resulting from the introduction of fix-dose combinations.

All these advances should not be confused with the fact that lifelong medical therapy will probably lead to substantial problems, especially in terms of adherence to therapy and possible long-term toxicities. With only 10 years of experience so far, the latter aspect has thus far only been captured in part. Infection with HIV should still be avoided at all costs. Apart from further improvement of ART and development of new therapeutic concepts such as eradication, a main focus of our endeavors must be the prevention of HIV in order to contain the further spread of disease.

The HIV epidemic

In 1981 the first three clinical descriptions of AIDS were published in the Morbidity and Mortality Weekly Report and later the New England Journal of Medicine. These reports described an epidemic of community-acquired Pneumocystis pneumonia, in most cases combined with oral thrush in previously healthy homosexual men, as well as chronic ulcerating perianal herpes infections (Gottlieb 1981a, Gottlieb 1981b, Masur 1981, Siegal 1981).

A little later, in June 1982, a notice from the Centers for Disease Control and Prevention (CDC) on three PCP cases among hemophiliacs was issued (CDC 1982a). In the same year a case of cryptosporidiosis in a hemophiliac patient from Pennsylvania (Eyster 1982) and an AIDS manifestation in an infant after a blood transfusion were reported (CDC 1982b). The occurrence of AIDS among hemophiliacs triggered a discussion of whether a viral infection could cause AIDS (Marx 1982). In particular, the similarity of populations at risk for AIDS and hepatitis B led to the hypothesis of a viral agent causing AIDS.

Studies on AIDS patients comprising different populations at risk quickly revealed common characteristics: compared to healthy controls, all AIDS cases had diminished counts of CD4-positive T lymphocytes. Conversely, a relative and absolute increase in CD8-positive T lymphocytes and a reduced mitogen-induced proliferative capacity of lymphocytes was observed (Gottlieb 1981, Masur 1981, Siegal 1981, Mildvan 1982, Stahl 1982). It became quickly clear, however, that the manifestation of AIDS was not a prerequisite for developing an immune deficiency. A defect of cellular immunity, associated with a generalized lymphadenopathy, had already been described very early in otherwise asymptomatic men who had sex with men (Kornfeld 1982, Stahl 1982). In January 1983 two cases of hemophiliacs with a lymphadenopathy syndrome were reported, both with significant dysfunction of cellular immunity (Ragni 1983). This led to the assumption that the lymphadenopathy syndrome and the observed cellular immune defects may have been precursors to AIDS and that a transmission of the AIDS causative agent via blood products was probable. Subsequently numerous studies on altered states of cellular immunity among hemophiliac patients were published. The main finding was a reduced CD4/CD8 ratio, the result of a relative and/or absolute decrease of CD4 lymphocyte counts together with elevated CD8 T cell counts. Only those patients who had been treated with small amounts of blood-clotting factors or where blood-clotting factors had been derived from small donor pools showed normal lymphocyte subpopulations (Luban 1983, Rasi 1984).

The altered immunological findings among hemophiliacs were discussed contraversially. In part they were attributed to a chronic antigen exposure due to the blood-clotting factor substitution. Other groups considered this hypothesis unlikely, given the fact that, prior to the advent of AIDS, no enhanced risk for infections was observed among hemophiliacs compared to other populations (except for viral infections, in particular hepatitis B and non-A-non-B-hepatitis via receipt of blood products). Overall, at that time no indication was seen to call into question the concept of blood-clotting substitution therapy among hemophiliacs (Anonymous 1983, Goldsmith 1983). As an alternative explanation of AIDS, particularly among the transmission group of men who have sex with men, coinfection with human cytomegalovirus, use of injection drugs, inhalation of amylnitrate (poppers) and exposure to foreign proteins (spermatozoa) were discussed (Essex 1997).

In 1983 different working groups raised the hypothesis that a variant of the T-lymphotropic retrovirus (HTLV-I), which had been discovered in 1980 by Gallo and colleagues, could be the causative agent of AIDS (Essex 1983, Gallo 1983). Several arguments were in favor of this hypothesis. At that time HTLV-I was the only known virus with the potential to infect human CD4-positive T lymphocytes (Poiesz 1980). In addition HTLV-I shared the same transmission routes with the potential AIDS agent, i.e., sexual contacts, blood-to-blood and perinatal transmission (Essex 1982).

First experiments to isolate virus related to HTLV-I or -II were only partially successful. Though cross-reactive antibodies with HTLV-related genome sequences were found in a small subset of AIDS patients, the overall assay reactivity was weak and suggested a coinfection with HTLV. The observations led to the assumption of a genetically more distant virus, one with weaker assay reactivity, as a putative etiologic agent. Indeed, only a short time later HTLV-III, later renamed Human Immunodeficiency Virus type I (HIV-1), was discovered as the causative agent of AIDS (Barré-Sinoussi 1983, Popovic 1984). In 2008 the French research group of Luc Montagnier and Francoise Barré-Sinoussi received the Nobel Prize in Medicine for their discovery of HIV-1.

Transmission routes

The main transmission routes of HIV are

  1. unsafe sex with an HIV-infected partner
  2. sharing injection paraphernalia with an HIV-infected partner
  3. vertical transmission of HIV from the HIV-infected mother to the newborn (before or at birth; or later, due to breastfeeding)

All other transmission routes, for the most part case reports, are notably rare. Among these are transmissions due to transfusion of blood or blood products in countries where blood donations are not routinely screened for HIV.

Extremely rare are transmissions due to contact with HIV-positive blood through open wounds or mucosa, or transmission of HIV after a bite (Bartholomew 2008). Recently three cases were reported where mothers infected their newborns probably via pre-chewed food (Gaur 2008). These transmission routes however are of a casuistic nature. Large case registries, in particular from the CDC, which have investigated into other transmission routes of HIV, clearly show that daily contacts of everyday life, such as the shared use of toilets or drinking from the same glass, cannot transmit HIV. Case registries in the health care setting, which analyze contact via saliva, urine, or infectious blood with intact skin, did not find a single transmission of HIV (Henderson 1990).

Potentially favorable factors and risks

Sex

The most important transmission route for HIV is sexual contact. The prerequisite for sexual transmission is direct exchange of infectious body secretions / fluids. The highest viral concentrations are found in blood and seminal fluid. A study investigating heterosexual transmission of HIV in female partners of HIV-positive hemophiliacs in Bonn found a seroconversion rate of HIV of 10% (Rockstroh 1995). The risk for sexual transmission was significantly higher if the HIV-positive partner suffered from advanced immunodeficiency or an advanced clinical stage of HIV infection. It is important to note that a precise calculation of transmission risk after one individual exposure is not possible. Various environmental factors have an influence on the actual transmission risk, such as specific sexual practices, concurrent sexually transmitted diseases, skin lesions, circumcision and mucosal trauma, that are difficult to take into account. The average transmission risks according to different sexual practices are shown in Table 1.

The correlation of transmission risk with the level of HIV viremia has important epidemiological implications. In environments where body fluids like blood and seminal fluid are exchanged with many persons over days or weeks, the risk of meeting people who have been recently infected, and thus who are highly infectious, is high. Likewise, the probability of infecting someone else between the transmission event and the detection of HIV antibodies is high. The later stage of disease is also a highly infectious,period, as HIV infection progresses and higher viral loads are again observed as one gets closer to falling below 200 CD4 T cells or AIDS. Sexually transmitted diseases and infections disrupt physiological skin and mucosal barriers and enhance the risk for HIV transmission. This is particularly true for endemic areas with a high prevalence of other sexually transmitted diseases. Primarily genital herpes lesions have been identified as a potential co-factor facilitating HIV transmission in endemic areas (Mahiane 2009).

Table 1. Likelihood for HIV transmission. (Modified from the guidelines  of the German and Austrian AIDS Society; please see also http://www.daignet.de)

Type of contact / partner

Probability of infection per contact

Unsafe receptive anal intercourse with HIV-positive partner

0.82% (95% CI 0.24 – 2.76)

Range 0.1 – 7.5%

Unsafe receptive anal intercourse with partner of unknown HIV serostatus

0.27% (95% CI 0.06 – 0.49)

Unsafe insertive anal intercourse with partner of unknown HIV serostatus

0.06% (95% CI 0.02 – 0.19)

Unsafe receptive vaginal intercourse

0.05 – 0.15%

Unsafe insertive vaginal intercourse

0.03 – 5.6%

Oral sex

No known probability, although case reports have been described, in particular after reception of seminal fluid into the mouth (Lifson 1990)

Note: 95% CI = Confidence Interval according to a large US HIV seroconverter Study (Vittinghoff 1999).

The observation that the level of HIV RNA is obviously critical in the infectiousness of an HIV-positive person, has recently initiated a controversial discussion regarding the possibility of a seropositive person having “safe” unprotected sex. The Swiss Commission for AIDS (Eidgenössische Kommission für AIDS-Fragen, EKAF) proposed to classify HIV-infected persons who are on ART with a plasma HIV RNA below the level of detection for at least 6 months, if they are adherent to therapy, regularly come to medical examinations, and if they do not have any signs of any other sexually transmitted diseases, as persons who most likely do not transmit HIV via sexual contact and therefore may have unprotected sex if they want (Vernazza 2008). The intention of the EKAF recommendation is to manage fears of HIV transmission and to enable a normal sex life, as far as possible, in persons with and without HIV. The EKAF recommendation is not agreed to by all HIV experts. Recently a case report from Frankfurt raised questions (Stürmer 2008), where HIV transmission occurred, though HIV viral load was not detectable and the HIV-positive partner was on successful ART (see chapter on Prevention).

Sharing injection paraphernalia

Sharing injection paraphernalia is the most important HIV transmission route for persons who use drugs intavenously. Due to the usually quite large amount of blood that is exchanged when sharing needles, the transmission risk is high. The aspiration of blood to control the correct intravenous position of the needle constitutes the reservoir for transmission. With the introduction of needle exchange programs, the installation of needle vendors, methadone substitution and multiple other preventive measures and social programs, HIV transmission rates have significantly decreased within intravenous drug users in Western Europe. In Eastern Europe, where intravenous drug use constitutes a criminal offence and no clean needles are provided, one sees an unyielding continual increase of HIV transmissions in this population. One can only hope that the success of prevention efforts in Western Europe will lead to a more liberal management and implementation of prevention programs in Eastern Europe.

Vertical transmission

Without intervention up to 40% of newborns born to HIV-1-positive mothers are infected with HIV-1. The most important risk factor is viral load at the time of delivery. Since 1995 the mother-to-child transmission rate of HIV-1-infected mothers has been reduced to 1 – 2%. These low transmission rates were reached through the combination of antiretroviral therapy / prophylaxis for the pregnant woman, elective caesarian section prior to the start of labor, the antiretroviral post-exposition prophylaxis for the newborn and substitution for breast feeding. For details refer to the chapter “HIV and Pregnancy” as well as to the European AIDS Clinical Society (EACS) guidelines for the clinical management and treatment of HIV-infected adults (HIV Med. 2008 Feb;9(2):65-71; please also visit the website http://www.europeanaidsclinicalsociety.org/).

Blood

The transmission of HIV via blood and blood products has been largely reduced on a global scale, though the risk is not completely eliminated. In Germany blood and blood products are considered safe. Since 1985 all blood donations are tested for HIV-1 via antibody tests, and since 1989 also against HIV-2. For a few years now blood donations are additionally tested via PCR to identify donors who may be in the window of seroconversion and where the HIV ELISA is still negative. Persons with so-called risk behavior, i.e., active injection drug users, sexually active men and women as well as immigrants from high-prevalence countries are excluded from blood donations

Occupationally-acquired HIV infection

The overall risk for HIV infection after a needlestick injury is estimated to be around 0.3%. The risk for HIV transmission is significantly higher if the injury occurred using a hollow needle – e.g., during blood withdrawal – than with a surgeon’s needle. For details on post-exposure prophylaxis (PEP) please refer to the respective chapter in this book. On the other hand, the risk of infecting a patient with HIV when the medical personnel is HIV-positive is extremely low. In 1993 19,036 patients of 57 HIV-infected physicians, dentists or medical students were screened for HIV infection (CDC 1993a). While 92 patients tested HIV-positive, none of the transmissions was related to the health practitioner.

Non-suitable transmission routes

In general, HIV-transmission due to day-to-day contact between family members is unlikely. It is important to avoid blood-to-blood contacts. Thus, razor blades or tooth brushes should not be commonly shared. In cases of cannula or needle usage, these should be safely deposited in appropriate sharps-containers and not be placed back into the plastic cover.

Insects

All studies that have investigated the possible transmission of HIV via insects have come to the same conclusion, that it is not possible. This holds true as well for studies performed in Africa with a high AIDS prevalence and large insect populations (Castro 1988).

The natural course of HIV infection

The natural course of HIV – in the absence of antiretroviral therapy – is shown in Figure 1. Shortly after infection a so-called acute retroviral syndrome is observed in some patients. This syndrome is characterized mainly by lymphadenopathy, fever, maculopapular rash, myalgia and usually does not last longer than four weeks (see chapter on Acute HIV Infection).

The symptoms are unspecific and variable so that the diagnosis of HIV infection is rarely made without additional testing. A period of several years follows where most patients are clinically asymptomatic.

Thereafter symptoms or diseases may occur, classified according to the CDC classification as category B (Table 2). Among these, oral thrush, oral hairy leukoplakia and herpes zoster are particularly noteworthy, and HIV infection as an underlying diagnosis should always be taken into account. Diseases of category B are not AIDS-defining, however their occurrence is defined as symptomatic of HIV infection and hints to a disturbed cellular immune system.

Still later in the course of HIV infection AIDS-defining illnesses occur at a median of 8–10 years after infection. Without highly active antiretroviral therapy these illnesses eventually lead to death after a variable period of time.

The level of HIV RNA, which reaches extremely high values shortly after primary infection, usually decreases to less than 1% of the maximum value at the time of first HIV antibodies and remains on a relatively stable level for a number of years. This level is called the viral set point. The level of the viral set point determines the speed of disease progression. While most patients with less than 1000 HIV RNA copies/ml are usually not affected by AIDS even 12 years after primary infection, more than 80% of patients have developed AIDS only 2 years after infection if the viral load remains at levels above 100,000 copies/ml (O’Brien 1996).

The higher the viral set point the faster the decrease of CD4 T cells. CD4 T cells usually drop considerably during acute primary infection. Subsequent CD4 counts recover after a few months to values within the normal range, though pre-infection values are rarely reached. Normal values for CD4 T cell counts vary from laboratory to laboratory, however these are usually in the range of absolute CD4-positive T lymphocytes in adults of 435–1600/µl or relative percentage between 31–60% of total lymphocytes. For children other values apply (see chapter on Pediatrics).

During the progressive course of HIV infection a gradual decrease of CD4 T cells is observed. The risk for AIDS-defining illnesses increases with time when CD4 T cells decrease below 200. To ascertain the level of immunodeficiency the relative percentage of CD4 T cells should also be taken into account.

Figure 1: The natural course of HIV infection
Table 2. Clinical categories of HIV infection according to CDC Classification

Category A

Asymptomatic HIV infection

·   Acute, symptomatic (primary) HIV ­in­fec­tion

·   Persistant generalized lymphade­nopa­thy (LAS)

Category B

Symptoms or signs of diseases that do not fall into Category C but are associated with a disturbed cellular immunity. Among these are:

·   Bacillary angiomatosis

·   Infections of the pelvis, in particular complications of fallopian tube or ovarian abscesses

·   Herpes zoster in the case of more than one dermatome or recurrence in the same dermatome.

·   Idiopathic thrombocytopenic pur­pura

·   Constitutional symptoms like fever or diarrhea lasting >1 month

·   Listeriosis

·   Oral hairy leukoplakia (OHL)

·   Oropharyngeal candidiasis (oral thrush)

·   Vulvovaginal candidiasis, either chronic (>1 mo­nth) or difficult to treat

·   Cervical dysplasia or car­cinoma in situ

·   Peripheral neuropathy

Category C

AIDS‑defining diseases

·   Candidiasis of the bronchia, trachea, or lungs.

·   Oesophageal candidiasis

·   CMV infections (except liver, spleen and lymph nodes)

·   CMV retinitis (with loss of vision)

·   Encephalopathy, HIV-related

·   Herpes simplex infections: chronic ulcer (>1 month); or bronchitis, pneumonia, oesophagitis

·   Histoplasmosis, disseminated or extrapulmonary

·   Isosporiasis, chronic, intestinal, duration >1 month

·   Kaposi sarcoma

·   Coccidioidomycosis, disseminated or extrapulmonary

·   Cryptococcosis, extrapulmonary

·   Cryptosporidiosis, chronic, intestinal, duration >1 month

·   Lymphoma, Burkitt

·   Lymphoma, immunoblastic

·   Lymphoma, primary CNS

·   Mycobacterium avium complex or M. kansasii, disseminated or extrapulmonary

·   Mycobacterium, other or not identified species

·   Pneumocystis pneumonia

·   Pneumonia, bacterial, recurrent (>2 within a year)

·   Progressive multifocal leukoencephalopathy

·   Salmonella Sepsis, recurring

·   Tuberculosis

·   Toxoplasmosis, cerebral

·   Wasting Syndrome

·   Cervix carcinoma, invasive

Under certain conditions (e.g., under myelosuppressive interferon therapy) low absolute CD4 T cell counts are observed in the context of leuko- and lymphopenia, while the immune status assessed by the relative CD4 T cell count remains normal. 200 CD4 T cells/µl correspond to approximately 15% of CD4 positive lymphocytes. Conversely, the absolute CD4 T cell count may suggest false high values, e.g., after a splenectomy.

Patients can be categorized depending on the speed of the CD4 T cell decrease (Stein 1997) to those with a high risk of disease progression (loss of more than 100 CD4 T cells/µl within 6 months), those with a moderate risk of disease progression (loss of 20–50 cells/µl per year) and those with a low risk of disease progression (loss of less than 20 cells/µl per year).

While the overall risk for AIDS increases if the CD4 T cell count drops below 200 cells/µl, considerable differences exist for the risk of individual AIDS manifestations (see chapter on AIDS). As an example, opportunistic infections usually occur at far lower CD4 T cell counts than AIDS-associated malignancies (Schwartländer 1992). Apart from the level of HIV RNA and CD4 T cell count, the age of the patient is another important risk factor for progression to AIDS (Figure 2). A 55-year-old patient with a CD4 T cell count of 50 cells/µl and an HIV RNA of 300,000 copies/ml has an almost twice as high risk of developing AIDS within six months as a 25-year-old patient. This explains why the latest antiretroviral treatment guidelines for HIV have included individual factors such as age and level of HIV viral load into their algorithms regarding when to start treatment.

In the pre-ART era the average time between the first manifestations of AIDS and death was 2–4 years. Without therapy probably more than 90% of all HIV patients die from AIDS. Today, the progression of HIV infection to AIDS can be halted with treatment. After reaching a maximal suppression of HIV RNA, CD4 T cell counts usually recover and patients regain an almost normal life expectancy.

The level of HIV RNA or the viral set point is dependent on a variety of host-specific factors such as HLA-type and other, as yet unidentified, factors. In addition, virus-related factors associated with HIV disease progression have to be taken into account.

Figure 2

It is important to visualize that the level of plasma viral load represents an equilibrium between new and dying HIV.

Disease progression stage

In order to classify the progression of HIV infection in most clinical settings the 1993 CDC classification is still being used that takes the clinical presentation and CD4 T cell count into account (Table 3).

Table 3: Classification of HIV disease according to the 1993 CDC classification

Symptoms /

CD4 T cells

Asymptomatic or acute HIV disease

Symptomatic but not stage A or C

AIDS-defining illness*

>500/µl

A1

B1

C1

200 – 499/µl

A2

B2

C2

<200/µl

A3

B3

C3

*for AIDS-defining conditions please refer to Table 2.

In 2008 a revised version of the CDC classification of HIV disease was presented. This revised version has been combined into a single case definition for adolescents ≥ 13 years and adults and is summarized in Table 4. Aim of the revised version was to introduce a simplified classification for continued epidemiological monitoring of HIV and AIDS, which refelected the improved diagnostics and treatment possibilities in the HIV field. In addition to the three stages listed below a fourth new stage (HIV infection, stage unknown) was introduced for patients in whom no CD4-counts or patient history were available.

Table 4: Classification of HIV-disease according to the 2008 classification

Stage

AIDS-defining illness*

CD4 T cell count

1

none

> 500/µl or ≥ 29%

2

none

200 – 499/µl or 14-28%

3 (AIDS)

Documented AIDS –defining illness

or < 200/µl or <14%

unknown

No information available

No information available

*the AIDS-defining illnesses have remained unchanged and are listed in table 2.

As a general rule for the classification of a patient, the stage is always adapted according to progression of disease (e.g., someone who is previously asymptomatic, CD4 T cell count 530/µl, they are a Category A; but if they develop oral thrush, their CD4 T cell count drops to 320/µl, they are Category B2). Reclassification upward upon improvement is not considered. If we take the same example as before and the patient has received fluconazole therapy and ART, and at present is asymptomatic and their CD4 T cells have returned to 550/µl the CDC stage remains at B2. The case definitions of the revised 2008 CDC classification are intended for public health surveillance and not as a guide for clinical diagnosis. Whereas in Europe the term AIDS is only used in cases of clinically manifest AIDS, in the US a CD4 T cell count below 200 cells/µl is also considered AIDS.

Epidemiology

The Human Immunodeficiency Virus probably emerged in the 1920s or ‘30s when the Simian Immunodeficiency Virus (SIV) jumped host from the chimpanzee to the human in Western Africa (Worobey 2008). The oldest HIV-positive human blood sample was found in Kinshasa (Zaire, now the Democratic Republic of Congo) and dates back to 1959 (Zhu 1998). After the first description of AIDS in 1981 by now almost all countries in the world have been affected by HIV.

The first to be infected are usually persons from so-called high-risk groups (intravenous drug users, professional sex workers, men who have sex with men) and subsequently other population groups are infected via unsafe sex. In industrialized countries homosexual sex is frequently the most common mode of transmission, whereas in countries of the former Soviet Union intravenous drug use (sharing injection paraphernalia) is the most common mode of transmission. In Africa most infections occur due to heterosexual intercourse.

Table 4: AIDS epidemic according to UNAIDS, 2010 (www.unaids.org)

HIV-infected adults and children

HIV prevalence among adults in 2009

New infections 2008

Yearly deaths due to AIDS 2009

Sub-Saharan-Africa

22,500,000

5.0%

1,800,000

1,300,000

Middle East and North Africa

460,000

0.2%

75,000

24,000

South and Southeast Asia

4,100,000

0.3%

270,000

260,000

East Asia

770,000

0.1%

82,000

36,000

Oceania

57,000

0.3%

4500

1,400

Latin America

1,400,000

0.5%

92,000

58,000

Caribbean

240,000

1.0%

17,000

12,000

Eastern Europe and Central Asia

1,400,000

0.8%

130,000

76,000

Western and
Central Europe

820,000

0.2%

31,000

8,500

North America

1,500,000

0.5%

70,000

26,000

Total

33,300,000

0.8%

2,600,000

1,800,000

The prevalence and subsequent implications on the epidemic are markedly different from country to country. Whereas HIV/AIDS constitutes a rather marginal health care problem in industrialized countries, in Sub-Saharan Africa AIDS has become the most common cause of death: every 5th death in Africa is due to AIDS. The overall life expectancy has decreased in some African states by more than 20 years. More than 10 million children have been orphaned. The economies of hard-hit states have and are continuing to suffer from dramatic slumps. According to UNAIDS, in 2009 around 33.3 million people were infected with HIV/AIDS worldwide (30.8 million adults, 16. million women ≥15 years and 2.5 million children under 15 years of age), approximately 2.6 million new HIV infections occurred and 1.8 million people died of AIDS (Table 4). Most profoundly affected countries are the regions of Sub-Saharan Africa, where more than 22,5 million people are infected with HIV. The highest dynamic of spread and incidence rates are currently observed in countries of the former Soviet Union, in particular Estonia, Latvia, Russia and the Ukraine, as well as in South and South-East Asia.

In Germany in 2010, around 70,000 people were HIV-positive (Table 6).

Table 6: Epidemiology of HIV/AIDS in Germany (modified according to http://www.rki.de)

Population

Total numbers (lower and upper estimate)

People with HIV/AIDS in 2010

70,000 (60,000–83,000)

Men

57,000 (49,000–68,000)

Women

13,000 (11,000–16,000)

Children

200

According to transmission group    

Men who have sex with men

42,000 (36,000–49,000)

Persons infected via heterosexual contacts

10,000 (8,700–12,000)

Persons from high prevalence regions / countries

7,300 (6,900-9,200)

Intravenous drug users

10,000 (8,500–12,000)

Hemophiliacs and received blood transfusions

500

Mother to child transmission

200

Summary

The first serological evidence for HIV infection was found in human sera from Zaire dating to 1959, Uganda dating back to1972 and Malawi to 1974 – evidence that HIV was circulating in Africa at those times. The first cases of AIDS were than described in the US in 1981. The discovery of HIV as the cause of AIDS was made in 1983. Since then HIV/AIDS has emerged as a worldwide epidemic which continues to spread today – 30 years later – with some 2.6 million new infections each year. In particular the high infection rates in Eastern Europe and Asia demonstrate the immense challenges that need to be met in current and future implementations of prevention measures. Even though the success of antiretroviral therapy in the treatment of HIV infection appears to enable a normal life expectancy for HIV-infected patients, knowledge on the natural course of HIV infection remains important. Not only in order to make the correct decision on when to start ART in an individual patient, but also to correctly diagnose HIV in patients with first symptoms of HIV infection who have not previously shown AIDS manifestations, this knowledge is important. In light of the fact that in Europe about 50% of all HIV-infected persons do not know their HIV status, tremendous challenges remain in the area of early diagnosis of HIV infection. Joint efforts are being made (www.HIVeurope2007.eu) in order to diagnose HIV infection earlier and thus enable physicians and patients to start ART on time, as well as to lower new infection rates by counseling patients on transmission modes and prevention.

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