The classification system used by the World Health Organization comprises four hierarchical clinical stages of HIV infection, ranging from stage 1 (asymptomatic) to stage 4 (AIDS) [1]. Patients showing at least one symptom attributed to a higher stage are assigned this higher stage. Also, they cannot be re-assigned a lower stage if symptoms are relieved by adequate treatment. This classification is to be understood as a one-way street and is described in detail in another article available on this platform, namely in the article dealing with HIV infection in general.

The clinical presentation of early-stage HIV infection is non-specific, and this applies to infections with either type of the virus. The majority of patients remains asymptomatic for years or develops persistent generalized lymphadenopathy. Individuals with HIV-2 infection tend to remain in this stage for even longer periods of time than those who acquired HIV-1 [2]. What's more, large shares of HIV-2 patients may be classified as long-term non-progressors who are not expected to show signs of immunodeficiency or disease for more than a decade [3] [4].

Those who do progress to advanced-stage HIV infection and AIDS develop similar symptoms, irrespective of the causative agent. Slight differences have been observed regarding the relative frequency of certain symptoms, but the clinical relevance of such data may be doubted. For the sake of completeness, they shall be briefly summarized here [3]:

• Chronic fever, which is generally attributed to stage 3, is less frequently observed in HIV-2 patients. By contrast, HIV-2 infection seems to predispose to chronic diarrhea due to bacterial infections. Mucocutaneous conditions such as oral candidiasis may be less common in patients with HIV-2.
• Stage 4 is defined by the occurrence of AIDS-defining illnesses, e.g., Kaposi sarcoma and wasting syndrome due to HIV. Kaposi sarcoma seems to be more typical of HIV-1 infection, while wasting syndrome is more frequently developed by those infected with HIV-2.

• Generalized Lymphadenopathy

  Persistent Generalized Lymphadenopathy (PGL) There is loss of normal lymph node architecture as the immune system fails with emergence from latency of HIV infection. It is marked by development of generalized lymphadenopathy. [library.med.utah.edu]

  The majority of patients remains asymptomatic for years or develops persistent generalized lymphadenopathy. Individuals with HIV-2 infection tend to remain in this stage for even longer periods of time than those who acquired HIV-1. [symptoma.com]

  Dysregulation of the IFN-I system has been suggested by us and others to contribute to different aspects of HIV-1 immunopathogenesis, including induction of CD4 T cell apoptosis, suppression of CD8 T cell responses, generalized lymphadenopathy, and promotion [jimmunol.org]

  Pépin J, Dunn D, Gaye I, Alonso P, Egboga A, Tedder R, et al. (1991) HIV-2 infection among prostitutes working in The Gambia: association with serological evidence of genital ulcer diseases and with generalized lymphadenopathy. [journals.plos.org]

• Burkina Faso

  FIT-2 is a multi-country, phase IIb, randomized, non-comparative study, carried out in West Africa (Côte d'Ivoire, Burkina Faso, Senegal, Togo). ARV-naïve HIV-2 infected adult patients will be recruited and followed during 96 weeks. [clinicaltrials.gov]

  Other West African countries reporting HIV-2 are Benin, Burkina Faso, Ghana, Guinea, Liberia, Niger, São Tomé, Senegal, and Togo. Angola and Mozambique are other African nations where the prevalence of HIV-2 is more than 1%. [webmd.com]

  References This article has been cited by 1 Characterization of HIV-1 genotypes and antiretroviral drug-resistanc mutations among patients in Burkina Faso Kagone, T.S., Hien, H., Meda, N., Diagbouga, P.S., Sawadogo, A., Drabo, J., Peeters, M., (...), [ijdvl.com]

  A total of 13 clinics (all are located in urban areas), in five countries (Benin, Burkina-Faso, Cote d’Ivoire, Mali, Senegal) are participating ( Figure 1 and Table 1 ). [journals.plos.org]

• Cape Verde

  Human immunodeficiency virus type 2 (HIV-2) infection is geographically restricted, affecting West African countries such as Guinea- Bissau and Cape Verde. We describe a recent case of HIV-2 infection in an Italian patient. [ncbi.nlm.nih.gov]

  West African nations with a prevalence of HIV-2 of more than 1% in the general population are Cape Verde, Côte d'Ivoire (Ivory Coast), Gambia, Guinea-Bissau, Mali, Mauritania, Nigeria, and Sierra Leone. [webmd.com]

  (The countries of origin representing ≥ 10 cases of HIV-2 infection included Ivory Coast, Ghana, Cape Verde, Gambia, Mali, Senegal, and Liberia.) Ninety-seven of the HIV-2 cases also had a positive HIV-1 Western blot antibody test result. [aetcnmc.org]

• Fever

  Other non-specific symptoms (including fever, night sweats and swollen lymph glands) are associated with progressive immune dysfunction. [hse.gov.uk]

  These are signs and symptoms of HIV infection: Sudden weight loss Night sweats or fever Extreme tiredness Swollen lymph nodes White spots in your mouth or throat Ongoing (chronic) diarrhea Pneumonia Reddish splotches on your skin or in your mouth Forgetfulness [urmc.rochester.edu]

  The symptoms of HIV infection and AIDS are usually the symptoms of the diseases that attack the body because of a weakened immune system: Fever that lasts from a few days to longer than a month Loss of appetite or weight, especially loss of more than [privatemdlabs.com]

  Response to treatment for HIV-2 infection may be monitored by following CD4+ T-cell counts and other indicators of immune system deterioration such as weight loss, oral candidiasis, unexplained fever, and the appearance of a new AIDS-defining illness. [ijdvl.com]

  Response to treatment for HIV-2 infection may be monitored by following CD4 + T-cell counts and other indicators of immune system deterioration, such as weight loss, oral candidiasis, unexplained fever, and the appearance of a new AIDS-defining illness [webmd.com]

• Candidiasis

  Response to treatment for HIV-2 infection may be monitored by following CD4+ T-cell counts and other indicators of immune system deterioration such as weight loss, oral candidiasis, unexplained fever, and the appearance of a new AIDS-defining illness. [ijdvl.com]

  Response to treatment for HIV-2 infection may be monitored by following CD4 + T-cell counts and other indicators of immune system deterioration, such as weight loss, oral candidiasis, unexplained fever, and the appearance of a new AIDS-defining illness [webmd.com]

  Mucocutaneous conditions such as oral candidiasis may be less common in patients with HIV-2. Stage 4 is defined by the occurrence of AIDS-defining illnesses, e.g., Kaposi sarcoma and wasting syndrome due to HIV. [symptoma.com]

  For example, conditions such as tuberculosis, esophageal candidiasis, wasting syndrome, cerebral toxoplasmosis, disseminated Mycobacterium avium intracellulare, cryptococcosis, cryptosporidiosis, cytomegalovirus disease, Kaposi's sarcoma, AIDS dementia [cid.oxfordjournals.org]

• Weight Loss

  These are signs and symptoms of HIV infection: Sudden weight loss Night sweats or fever Extreme tiredness Swollen lymph nodes White spots in your mouth or throat Ongoing (chronic) diarrhea Pneumonia Reddish splotches on your skin or in your mouth Forgetfulness [urmc.rochester.edu]

  Response to treatment for HIV-2 infection may be monitored by following CD4+ T-cell counts and other indicators of immune system deterioration such as weight loss, oral candidiasis, unexplained fever, and the appearance of a new AIDS-defining illness. [ijdvl.com]

  Response to treatment for HIV-2 infection may be monitored by following CD4 + T-cell counts and other indicators of immune system deterioration, such as weight loss, oral candidiasis, unexplained fever, and the appearance of a new AIDS-defining illness [webmd.com]

  ARC patients usually show symptoms of fatigue, weight loss, and night sweats, along with superficial fungal infections of the mouth (oral thrush) and fingernails and toenails (onychomycosis). [library.med.utah.edu]

• Sore Throat

  throat Long-lasting or multiple viral skin problems, such as herpes sores or plantar warts Repeated, severe yeast infections in your mouth or vagina despite treatment Chronic muscle and joint pain Diarrhea, especially if it lasts longer than a month [privatemdlabs.com]

• Pharyngitis

  Prospective studies of acute HIV infections show that fever, lymphadenopathy, pharyngitis, diffuse erythematous rash, arthralgia/myalgia, diarrhea, and headache are the commonest symptoms seen with acute HIV infection. [library.med.utah.edu]

• Diarrhea

  These are signs and symptoms of HIV infection: Sudden weight loss Night sweats or fever Extreme tiredness Swollen lymph nodes White spots in your mouth or throat Ongoing (chronic) diarrhea Pneumonia Reddish splotches on your skin or in your mouth Forgetfulness [urmc.rochester.edu]

  Tiredness Prolonged swelling of the lymph nodes Sore throat Long-lasting or multiple viral skin problems, such as herpes sores or plantar warts Repeated, severe yeast infections in your mouth or vagina despite treatment Chronic muscle and joint pain Diarrhea [privatemdlabs.com]

  By contrast, HIV-2 infection seems to predispose to chronic diarrhea due to bacterial infections. Mucocutaneous conditions such as oral candidiasis may be less common in patients with HIV-2. [symptoma.com]

  Prospective studies of acute HIV infections show that fever, lymphadenopathy, pharyngitis, diffuse erythematous rash, arthralgia/myalgia, diarrhea, and headache are the commonest symptoms seen with acute HIV infection. [library.med.utah.edu]

• Chronic Diarrhea

  These are signs and symptoms of HIV infection: Sudden weight loss Night sweats or fever Extreme tiredness Swollen lymph nodes White spots in your mouth or throat Ongoing (chronic) diarrhea Pneumonia Reddish splotches on your skin or in your mouth Forgetfulness [urmc.rochester.edu]

  By contrast, HIV-2 infection seems to predispose to chronic diarrhea due to bacterial infections. Mucocutaneous conditions such as oral candidiasis may be less common in patients with HIV-2. [symptoma.com]

• Vomiting

  […] and AIDS are usually the symptoms of the diseases that attack the body because of a weakened immune system: Fever that lasts from a few days to longer than a month Loss of appetite or weight, especially loss of more than 10% of body weight Nausea and vomiting [privatemdlabs.com]

• Arthralgia

  Prospective studies of acute HIV infections show that fever, lymphadenopathy, pharyngitis, diffuse erythematous rash, arthralgia/myalgia, diarrhea, and headache are the commonest symptoms seen with acute HIV infection. [library.med.utah.edu]

• Night Sweats

  These are signs and symptoms of HIV infection: Sudden weight loss Night sweats or fever Extreme tiredness Swollen lymph nodes White spots in your mouth or throat Ongoing (chronic) diarrhea Pneumonia Reddish splotches on your skin or in your mouth Forgetfulness [urmc.rochester.edu]

  Other non-specific symptoms (including fever, night sweats and swollen lymph glands) are associated with progressive immune dysfunction. [hse.gov.uk]

  ARC patients usually show symptoms of fatigue, weight loss, and night sweats, along with superficial fungal infections of the mouth (oral thrush) and fingernails and toenails (onychomycosis). [library.med.utah.edu]

• Encephalopathy

  Two patients experienced complications from HIV, one patient had HIV encephalopathy and molluscom contagiosum, and another had microsporidiosis infection in the setting of AIDS. [ncbi.nlm.nih.gov]

  In some cases, infection of the central nervous system occurs, often leading to progressive brain damage (encephalopathy). Several different conditions may occur as a result of HIV infection that precedes the development of AIDS. [hse.gov.uk]

  Pathology 03/13/2014 Electron Microscopy, Tissue (HCMC) Pathology 06/01/2017 Electron Microscopy, Whole Blood Pathology 02/04/2016 Emergency Transfusion Transfusion Services 09/03/2014 Emergency Use of Blood Components Transfusion Services 02/20/2019 Encephalopathy [childrensmn.org]

Routine testing doesn't aim at an immediate confirmation of HIV-2 infection but rather strives for the clarification of an individual's general HIV status. Both direct and indirect assays may be used to confirm HIV infection, and they primarily differ in their window periods [5]:

• The very early detection of HIV infection is based on the amplification and identification of viral RNA. Nucleic acid amplification tests are generally stated to yield reliable results within 1-2 weeks after the acquisition of the pathogen, but HIV-2 viral loads have been shown to be below the measuring threshold in 25-40% of antiretroviral naïve patients [2] [6].
• Viral antigen becomes detectable from the third week of infection. The majority of assays, however, is oriented towards the recognition of HIV-1 core protein p24. The respective antigen of HIV-2 is p26, and standard immunoassays may have a lower sensitivity for the detection of p26, which may imply a longer window period. One possible solution to this issue is the inclusion of HIV-2-specific targets in antigen assays, such as HIV-2 envelope glycoprotein gp36.
• The production of antibodies may not be confirmed until >3 weeks after primary exposure, but serology is a mainstay of standard HIV testing. Care should be taken, though, when interpreting serological assays with regard to the type of HIV infection: Cross-reactivity of antibodies against HIV-2 is a well-known phenomenon often leading to dual reactivity, although co-infections with HIV-1 and HIV-2 account for a minority of cases only [2]. By contrast, the identification of pure HIV-1 infection doesn't usually pose any problems, presumably because sensitivity and specificity have been optimized for this type of infection [6] [7].

HIV type discrimination ideally relies on the results of both nucleic acid amplification and immunological tests [6]. This approach allows for a certain compensation of limitations in sensitivity (due to low HIV-2 viral loads and antigenic differences) and specificity (due to the cross-reactivity of antibodies against HIV-2).

The confirmation of HIV-2 infection entails an extensive laboratory workup to assess the patient's immune status, and to check for co-infections. This workup follows the general recommendations for HIV infection and includes [8]:

• Quantification of HIV loads
• HIV genotyping and test for drug-resistance, if feasible
• Complete blood count and chemistry panel, including CD4+ T-cell counts with percentage
• Fasting lipid profile
• Baseline urinalysis and calculated creatinine clearance or estimated glomerular filtration rate
• Screening for glucose-6-phosphate dehydrogenase deficiency
• HLA B*5701 screening
• Test for infections with Mycobacterium tuberculosis, hepatitis B virus, hepatitis C virus, Toxoplasma gondii
• Test for other sexually transmitted diseases like syphilis and Chlamydia infection

Adequate treatment should be provided as soon as HIV infection is diagnosed, irrespective of the presence of symptoms. This applies to both genders and all ages, including pregnant women. The World Health Organization has published Consolidated Guidelines on the Use of Antiretroviral Drugs for Treating and Preventing HIV Infection [1], but these guidelines are mainly focused on the management of the much more common HIV-1 infection. Similarly, most antiretroviral drugs have been designed for the treatment of HIV-1 infection, and HIV-2 carries intrinsic resistance to several compounds.

Neither non-nucleoside reverse transcriptase inhibitors (e.g., efavirenz and nevirapine) nor the fusion inhibitor enfuvirtide should be administered to HIV-2 patients [9], although these drugs are part of most first-line regimens as described in the aforementioned guidelines [1]. Reduced susceptibility to protease inhibitors like amprenavir has also been shown for HIV-2 and may be confirmed by means of drug-resistance testing [9]. Taking into consideration these peculiarities of HIV-2, clinical trials have been carried out to assess the effects of integrase-inhibitor-based regimens:

• Raltegravir, emtricitabine, and tenofovir disoproxil fumarate, in adult patients [10]
• Elvitegravir, cobicistat, emtricitabine, and tenofovir disoproxil fumarate, in adults infected with HIV-2 [11]

The authors of both studies concluded these regimens to be effective, safe, and well-tolerated. Alternative single-tablet regimens with expected effectiveness in HIV-2 infection are listed elsewhere [2], and some of them may possibly be employed in pregnant women, adolescents, or children. However, reliable data is lacking to establish a preferred antiretroviral therapy regimen in these patient groups.

Lifelong treatment is required, and patients should be monitored for their response to ART. Six and twelve months after the initiation of ART, and annually thereafter, HIV loads should be measured, and CD4+ T-cell counts should be evaluated to assess the patient's immune status. These tests may be complemented by standard analyses of blood samples to detect potential signs of organ failure [1].

Patients with HIV-2 infection have a better prognosis than those with HIV-1 infection, although the reasons for these difference remain poorly understood [3]. There is a tendency towards lower viral loads and higher CD4+ T-cell counts in HIV-2 patients, even in advanced stages of the disease. These parameters may thus not reliably predict the outcome if compared with reference values mainly obtained from HIV-1 patients. In general, both long-term non-progressors and those with higher viral loads who receive effective ART have a near-to-normal life expectancy.

Upon the onset of AIDS-defining illnesses, median survival times of patients infected with HIV-1 and HIV-2 are six and twelve months, respectively [3].

The Simian Immunodeficiency Virus of sooty mangabeys (Cercocebus atys) has been identified as the origin of HIV-2 [9]. In detail, two independent transmission events, which possibly occurred at the beginning of the 20th century, yielded HIV-2 groups A and B, which differ in genetics, pathogenicity, and virulence. According to a study realized in Portugal, HIV-2 group A accounts for up to 97% of cases [12]. Another seven groups of HIV-2 have been described in single patients only. The hunting of sooty mangabeys, the consumption of their meat, and their use as pets may have provided multiple opportunities for cross-species transmission [9].

The routes of transmission of HIV-2 are not different from those described for HIV-1 and mainly comprise the exposure to blood and body fluids during sexual intercourse, needle sharing, and the transfusion or transplantation of blood and organs, as well as vertical transmission in utero, peripartum, or during breastfeeding [13] [14]. The overall risk of transmission is significantly lower for HIV-2, which is due to lower viral loads in blood and body fluids as well as lower genital shedding [2] [9]. For instance, the risk of mother-to-child transmission has been estimated at <2% and 10-40% for HIV-2 and HIV-1, respectively [15].

The origin of HIV-2 has been located in the Taï forest in Ivory Coast, West Africa [9]. And while HIV-2 infection may be diagnosed worldwide, the majority of cases is still reported in West Africa. HIV-2 group A is distributed throughout the entire region, and HIV-2 group B is mainly found in Ivory Coast, Ghana, Burkina Faso, and Mali. In sum, about 1-2 million people may have been infected in 2007, with more recent figures not being available. The percentage share of HIV-2 infections may reach 20% in West African nations, but is estimated at <5% in Portugal and France, and <1% in all other countries.

The detrimental consequences of HIV infection are due to the gradual loss of CD4+ T-cells and imbalance in CD4+ T-cell homeostasis, resulting in progressive immunodeficiency and ultimately death. CD4+ T-cells are implicated in cellular and humoral immune responses against infections, and they are selectively infected by HIV. The virus binds to CD4 and enters the target cell, replicates inside the lymphocyte and eventually induces host cell lysis or the formation of syncytia with uninfected T cells. Either way, additional cells will become infected with the virus.

The spread of the infection is associated with decreasing quantities of CD4+ T-cells and a reduction in the number of functional cells, but this process seems to run rather slow in HIV-2 infection. CD4+ T-cell counts diminish at a smaller rate than those observed in HIV-1 patients, which may be due to a more efficient immunological response and lower replication efficiency in primary cells. Dendritic cells, for instance, do not normally get activated and are not efficiently infected by HIV-1 but by HIV-2 [4].

There is no vaccine to prevent HIV-2 infection, and little work is done to this end. Considerable research is underway to develop an effective and safe HIV-1 vaccine, but even if these efforts come to fruition, such a product is unlikely to provide cross-protection for HIV-2 [2]. Accordingly, information campaigns and sex education remain the pillars of prophylaxis of this sexually transmitted disease. The correct and consistent use of condoms largely reduces the risk of infection, as does the reduction of the number of sexual partners. Before abstaining from condoms, both partners should get tested for HIV infection. At the community level, condoms may be provided to those who are unable or unlikely to purchase them, needle and syringe programs may be implemented to diminish the spread of the virus among drug addicts, and blood, tissues, and organs to be transplanted to another person should always be screened for the presence of HIV [1].

Additionally, people at very high risk of exposure to HIV may be provided pre-exposure prophylaxis containing tenofovir disoproxil fumarate [1]. This may apply to serodiscordant couples, heterosexual men and women, men who have sex with men, transgender people, sex workers, people who inject drugs, and those in prisons and other closed settings. Although there are no trials regarding the effectivity of pre-exposure prophylaxis of HIV-2 infection, HIV-2 is susceptible to all nucleoside reverse transcriptase inhibitors currently approved for HIV-1 treatment, including tenofovir disoproxil fumarate [2]. Similarly, post-exposure prophylaxis as applied to prevent HIV-1 infection is likely to be effective in the
prevention of HIV-2 transmission.

HIV infection may be caused by either of two related, yet distinct retroviruses: by HIV-1 and HIV-2. HIV-2 has first been isolated in 1986, namely from two patients originating from West Africa [16]. It has been speculated to have been circulating in West Africa since at least 1966, and the reduced virulence of this type of HIV is commonly mentioned as the main reason for it remaining undetected for decades. HIV-2 infection usually involves a longer asymptomatic stage and the decline in CD4+ T-cell counts is slower. The risk of horizontal and vertical transmission is lower, as is AIDS-related mortality [2].

Human immunodeficiency virus (HIV) infection is possibly the most widely known sexually transmitted disease. It follows a progressive course and is associated with a gradual impairment of the immune system, eventually leading to life-threatening acquired immunodeficiency syndrome (AIDS) and death. There are two types of HIV, namely HIV-1 and HIV-2. The latter accounts for a minority of infections and is most commonly found in West Africa. HIV-2 is generally considered to be less virulent than HIV-1: Patients infected with HIV-2 may remain in the asymptomatic stage of the disease for decades. Still, progression to AIDS is possible and should be avoided by adequate treatment.

The routes of transmission don't differ between HIV-1 and HIV-2, and neither does the clinical presentation. Specific tests need to be run in order to distinguish between both types of the virus and to choose the most effective treatment regimen. In sum, the general recommendation to seek medical advice in case of suspected exposure to HIV should be followed irrespective of the type of the virus.

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3. Nyamweya S, Hegedus A, Jaye A, Rowland-Jones S, Flanagan KL, Macallan DC. Comparing HIV-1 and HIV-2 infection: Lessons for viral immunopathogenesis. Rev Med Virol. 2013; 23(4):221-240.
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