|
| A) | 37.7 million | ||
| B) | 56.2 million | ||
| C) | 75.4 million | ||
| D) | 1.2 billion |
According to the World Health Organization (WHO), an estimated 37.7 million individuals worldwide were living with HIV by the end of 2020, of whom more than two-thirds (25.4 million) were in the WHO African Region [5]. Northern Africa, the Middle East, and eastern Europe and central Asia (particularly the Russian Federation) have had the fastest growing epidemics—new HIV infections in these regions have approximately doubled in the past 20 years. In 2020, an estimated 680,000 people died from HIV-related causes and 1.5 million people acquired HIV infection [5]. It is important to note that despite increases in certain geographic areas and demographic groups, overall, the rate of new infections was declining prior to the COVID-19 pandemic. Service disruptions during COVID-19 have slowed the pace of public health response to HIV, raising concern that increasing HIV infections and excess HIV-related deaths may erode the progress made in sub-Saharan Africa [5].
| A) | 55% | ||
| B) | 62% | ||
| C) | 78% | ||
| D) | 95% |
As of 2019, the Centers for Disease Control and Prevention (CDC) report several statistics and trends in the HIV/AIDS epidemic [9]:
By region, the prevalence rates are 50% higher in the Northeast and South (525 per 100,000) than in the West (365 per 100,000) and Midwest (253 per 100,000).
By race/ethnicity, 40% are Black/African American, 28% White, 25% Hispanic, and less than 1% are American Indian/Alaska Native or Asian/Pacific Islander.
By sex at birth, 78% of adults and adolescents living with HIV are male.
| A) | depletion of helper T cells. | ||
| B) | decreased suppressor T cells. | ||
| C) | increased killer T cell activity. | ||
| D) | elevated T lymphocyte functional capacity. |
Once the virus enters the cell, it may replicate, induce cell fusion and propagation of infection, or lead to cell death [12]. HIV targets the immune system, and the defining characteristic of HIV disease is progressive immunodeficiency caused by ongoing viral replication and cell-to-cell transmission within lymphoid tissue. With chronicity there is a progressive depletion of CD4 (helper-inducer) lymphocytes, the very T lymphocyte cohort whose function it is to direct other cells in the immune system, and to orchestrate the inactivation of virus antigen. The result is a depressed T lymphocyte functional capacity, characterized by depletion of helper T cells (T4), impaired killer T cell activity, and increased suppressor T cells (T8). Eventually, impaired immunity renders the individual vulnerable to opportunistic infection and certain malignancies. The common laboratory measure of immune function is the CD4 cell count. In persons with intact lymphocyte immune systems, the normal number of CD4 T cells ranges from 600–1,200 cells/mcL, depending on the stage and duration of infection.
| A) | less than 12 to 24 hours. | ||
| B) | less than 14 days. | ||
| C) | 21 days. | ||
| D) | more than 2 months. |
The clinical manifestations of HIV disease are determined by the stage of primary infection and the chronicity and degree of the resultant cellular immunodeficiency state. Acute, primary HIV infection may be asymptomatic, but most often it is manifest by a subacute viral syndrome of malaise and fatigue, fever, sore throat, rash, myalgia, headache, and lymphadenopathy—clinical features similar in many respects to that seen with Epstein-Barr virus mononucleosis, cytomegalovirus (CMV), and certain types of herpes simplex infections [12]. A variety of atypical symptoms and signs may be seen, including aseptic meningitis syndrome, genital ulcers, and ulcerations involving the gingiva, palate, or buccal mucosa. The acute illness usually resolves in less than 14 days but may follow a protracted course over many weeks [12].
| A) | 50 cells/mcL. | ||
| B) | 500 cells/mcL. | ||
| C) | 5,000 cells/mcL. | ||
| D) | 50,000 cells/mcL. |
Without satisfactory antiretroviral therapy, the usual patient with HIV/AIDS experiences a slow, inexorable wasting illness punctuated by periods of feverishness and diarrhea, becoming increasingly anorectic, malnourished, and lethargic. Late clinical signs include muscle wasting and weakness, anemia and thrombocytopenia, lymphadenopathy, pulmonary infiltrates, and neurologic abnormalities (such as dementia, peripheral neuropathy, and tremors). The median survival of patients with advanced HIV/AIDS (CD4 count <50 cells/mcL) is approximately 12 to 18 months. Patients succumb to complications of uncontrolled infection, malignancy, or critical organ failure (such as uremia or adrenal insufficiency).
| A) | MSM | ||
| B) | IDUs | ||
| C) | Close contact | ||
| D) | Perinatal transmission |
On the basis of newly reported cases, the transmission categories are [10]:
Male-to-male sexual contact (MSM)
Injecting drug users (IDUs)
MSM who inject drugs
Heterosexual contact
Perinatal transmission
Other (includes hemophilia, blood transfusion, and risk factor not reported or not identified)
| A) | Oral sex | ||
| B) | Unprotected vaginal intercourse | ||
| C) | Protected insertive anal intercourse | ||
| D) | Unprotected receptive anal intercourse |
Posing the highest risk of infection is unprotected anal receptive intercourse, followed by unprotected vaginal intercourse and unprotected insertive anal intercourse (particularly for uncircumcised men) [19,20]. Risk is reduced through the use of latex condoms. For the wearer, latex condoms provide a mechanical barrier limiting penile exposure to infectious cervical, vaginal, vulvar, or rectal secretions or lesions. Likewise, the partner is protected from infectious pre-ejaculate, semen, and penile lesions. Oil-based lubricants may make latex condoms ineffective and should not be used; water-soluble lubricants are considered safe. Natural membrane condoms (made from lamb cecum) contain small pores and do not block HIV passage. It is estimated that latex condom use reduces the risk of HIV transmission by approximately 70% to 80% [21,22,23]. Although abstinence from sexual contact is the sole way to absolutely prevent transmission, sexual activity in a mutually monogamous relationship in which neither partner is HIV-infected and no other risk factors are present is considered safe [4]. However, men who identify publicly as heterosexual and generally have committed relationships with women, but who also engage in sexual activity with other men, may be a transmission bridge to heterosexual women [24]. To better understand the actual extent of this behavior and its impact on HIV transmission, more research is necessary.
| A) | medication-assisted drug treatment. | ||
| B) | free provision of sterile injection equipment. | ||
| C) | recruitment of "street" outreach workers for intensive drug and sex risk-reduction educational campaigns. | ||
| D) | All of the above |
Transmission of HIV among IDUs occurs primarily through contamination of injection paraphernalia with infected blood. The risk of sustaining HIV infection from a needle stick with infected blood is approximately 1 in 300 [30]. Behavior such as needle sharing, "booting" the injection with blood, and performing frequent injections increases the risk. Crack cocaine use (by injection or smoking) is associated with a higher prevalence of HIV infection. This may in part be attributed to the exchange of cocaine for sex. Sharing of equipment is common due to legal and financial restrictions and cultural norms, and some studies have linked higher levels of psychologic distress (e.g., anxiety and depressive symptoms) with an increased risk for needle sharing [31]. Secondary transmission occurs to children and sexual partners. Preventative strategies include medication-assisted drug treatment, onsite medical care in a drug treatment program, recruitment of "street" outreach workers for intensive drug and sex risk-reduction educational campaigns, teaching addicts to sterilize their equipment between use, the free provision or exchange of sterile injection equipment (as allowed by law), distribution of condoms and bleach to clean drug use equipment, or a combination of these interventions.
| A) | only after tests have confirmed infection. | ||
| B) | after three consecutive positive test results. | ||
| C) | as soon as possible and continued for four weeks. | ||
| D) | after 24 to 48 hours and continued for at least eight weeks. |
The 2018 updated PHS guidelines recommend initiating PEP medication as soon as possible after occupational exposure to HIV and to continue the regimen for four weeks. PEP regimens should contain three (or more) antiretroviral drugs for all occupational exposures to HIV [39]. Examples of recommended PEP regimens include those consisting of a dual nucleoside reverse transcriptase inhibitor (NRTI) backbone plus an integrase strand transfer inhibitor (INSTI), protease inhibitor (PI) (boosted with ritonavir), or non-nucleoside reverse transcriptase inhibitor (NNRTI). The PHS preferred regimen for management of most healthcare professionals' exposures to HIV is emtricitabine and tenofovir dispensed together as Truvada, a fixed-dose combination tablet, 1 mg once daily, plus raltegravir, 400 mg twice daily [39]. This preparation is available as a starter packet that should be stocked at every healthcare facility where exposure to HIV is possible. As discussed, the regimen has been selected for its tolerability and safety profile. There are several alternative regimens that may be selected due to individual patient concerns. For example, tenofovir is associated with renal toxicity, and an alternative NRTI/NNRTI pair, such as zidovudine plus lamivudine (available as Combivir), would be selected for patients with renal disease [39].
| A) | Acute HIV infection often produces symptoms of an infectious mononucleosis-like illness. | ||
| B) | Laboratory abnormalities include lymphopenia, atypical lymphocytosis, and decreased CD4 count. | ||
| C) | The degree of plasma viral load six months following primary infection will have little influence on the subsequent pace of disease progression. | ||
| D) | Left untreated, HIV causes a protracted infection of the immune system with an average annual decrease in CD4 count of about 50 cells/mcL. |
As discussed, HIV infection is a protracted illness that passes through several stages and, if untreated, carries an 80% mortality rate at 10 years. Within 15 to 30 days after acquisition of HIV infection, the majority of patients (50% to 90% in reported series) develop an acute retroviral syndrome similar to infectious mononucleosis [12]. Symptoms include fever, sore throat, malaise, rash, diarrhea, lymphadenopathy, mucocutaneous ulcerations and weight loss averaging 10 pounds. A variety of neurologic syndromes including encephalitis may occur. The illness is self-limited, with an average duration of two to three weeks. Laboratory abnormalities include lymphopenia, atypical lymphocytosis, thrombocytopenia, and a decreased CD4 cell count. During this early phase of clinical illness, HIV antibody tests are often negative and the diagnosis rests on the demonstration of HIV P24 antigen or, preferably, quantitative plasma HIV RNA. Concentrations of HIV RNA in the blood (viral load) are high during the acute syndrome.
Following the host immune response, coincident with seroconversion and the rise in CD8 cytotoxic T cells, the viral load decreases steadily, reaching a relatively stable level at about six months. At this juncture, the degree of viral load correlates with the subsequent pace of disease progression. Patients having the highest viral loads, exhibit the most rapid progression to AIDS. As a result of the ongoing, protracted infection of target lymphocytes, the CD4 count gradually declines over time in the absence of treatment, at the average annual rate of about 50 cells/mcL.
| A) | Candidiasis | ||
| B) | Oral herpes | ||
| C) | Kaposi sarcoma | ||
| D) | Pneumocystis jiroveci pneumonia |
Chronic, asymptomatic HIV infection with ongoing low-level viral activity may last for many years before eventual progression to AIDS. Symptomatic illness can be expected to supervene as the CD4 count declines to a level less than 200 cells/mcL, as this correlates with severe immunodeficiency. The CDC defines late-stage HIV infection as AIDS on the basis of two criteria: CD4 count less than 200 cells/mcL or a characteristic AIDS-defining illness such as PJP, central nervous system (CNS) toxoplasmosis, or other opportunistic infections or tumors (Kaposi sarcoma). A variety of clinical syndromes may supervene at this juncture including dementia, peripheral neuropathy, wasting syndrome, and chronic diarrhea. In the United States, the most common AIDS-defining opportunistic diseases are: PJP, Kaposi sarcoma, candidiasis, cryptococcosis, cryptosporidiosis, CMV, atypical mycobacteriosis, systemic herpes, toxoplasmosis, and tuberculosis [41].
| A) | Abacavir | ||
| B) | Tipranavir | ||
| C) | Enfuvirtide | ||
| D) | Lamivudine |
Development of mature infectious virus depends upon enzymatic cleavage of HIV transcribed polyprotein by HIV protease. In binding to the active site of the HIV protease, PIs interrupt the formation of mature infectious particles and reduce viral replication by as much as 99%. Resistance to PIs develops rapidly when these agents are used alone. However, in combination with nucleoside analogs the effect can last for years, often resulting in a reduction of viral load to undetectable levels. Available agents include: ritonavir (Norvir, RTV); saquinavir (Invirase, Fortovase, SQV); atazanavir (Reyataz, ATZ); tipranavir (Aptivus, TPV); darunavir (Prezista; DRV); and fosamprenavir (Lexiva, FPV) [43].
| A) | three NNRTIs. | ||
| B) | two FIs and an NRTI. | ||
| C) | two PIs and a pharmacokinetic enhancer. | ||
| D) | two NRTIs in combination with an INSTI, an NNRTI, or a PI. |
For treatment-naïve patients, initial recommended therapy generally consists of two NRTIs in combination with a third active antiretroviral drug from one of three drug classes: an INSTI, an NNRTI, or a PI with a pharmacokinetic enhancer (cobicistat or ritonavir) [42]. These regimens result in maximum reduction of viral load for the longest period of time. When used as initial therapy, these regimens will achieve the goal of no detectable virus in the majority of patients after four to six months [42].
| A) | fluconazole 400 mg daily. | ||
| B) | voriconazole 200 mg daily. | ||
| C) | revaccination with a second vaccine series. | ||
| D) | one dose of benzathine penicillin G 2.4 million units IM. |
PROPHYLAXIS TO PREVENT FIRST EPISODE OF OPPORTUNISTIC DISEASE AMONG ADULTS AND ADOLESCENTS INFECTED WITH HIV
| Pathogen | Indication | Preventive Regimen | |
|---|---|---|---|
| Preferreda | Alternative | ||
| Pneumocystis jiroveci pneumonia (PJP) | CD4 count <200 cells/mcL (AI); or oropharyngeal candidiasis (AII), or CD4 <14% (BII); or history of AIDS-defining illness (BII), or CD4 count >200 but <250 cells/mcL if monitoring CD4 cell count every three months is not possible (BII) | Trimethoprim-sulfamethoxazole (TMP-SMZ) 1 double-strength (DS) daily (AI), or TMP-SMX 1 single-strength (SS) daily (AI) | TMP-SMX 1 DS three times weekly (TIW) (BI); or dapsone 100 mg daily or 50 mg twice daily (BI); or dapsone 50 mg daily + pyrimethamine 50 mg + leucovorin 25 mg weekly (BI); or dapsone 200 mg + pyrimethamine 75 mg + leucovorin 25 mg weekly (BI); or aerosolized pentamidine 300 mg via Respirgard II nebulizer every month (BI); or atovaquone 1,500 mg daily (BI); or atovaquone 1,500 mg + pyrimethamine 25 mg + leucovorin 10 mg daily (CIII) |
| Toxoplasma gondii encephalitis | Toxoplasma immunoglobulin G (IgG)-positive patients with CD4 count <100 cells/mcL (AII). Seronegative patients receiving PJP prophylaxis not active against toxoplasmosis should haveToxoplasmaserology retested if CD4 count decline to <100 cells/mcL (CIII). Prophylaxis should be initiated if seroconversion occurred (AII). | TMP-SMX 1 DS daily (AII) | TMP-SMX 1 DS TIW (BIII); or TMP-SMX 1 SS daily (BIII); or dapsone 50 mg daily + pyrimethamine 50 mg + leucovorin 25 mg weekly (BI); or dapsone 200 mg + pyrimethamine 75 mg + leucovorin 25 mg weekly (BI); or atovaquone 1,500 mg daily (CIII); or atovaquone 1,500 mg + pyrimethamine 25 mg + leucovorin 10 mg daily (CIII) |
| Latent Mycobacterium tuberculosis infection (LTBI) | A positive screening test for LTBI, with no evidence of active TB and no prior treatment for active TB or LTBI (AI); or close contact with a person with infectious TB, regardless of screening test results (AII) | Isoniazid (INH) 300 mg + pyridoxine 25 mg daily for nine months (AII); or INH 900 mg biweekly (by direct-observation therapy) + pyridoxine 25 mg daily for nine months (BII). | Rifampin 600 mg daily for four months (BIII); or rifabutin (dose adjusted based on concomitant ART) for four months (BIII). For drug-resistant TB, consult an expert or public health authorities (AII). |
| Disseminated Mycobacterium avium complex (MAC) disease | CD4 count <50 cells/mcL after ruling out active disseminated MAC disease based on clinical assessment (AI) | Azithromycin 1,200 mg once weekly (AI); or clarithromycin 500 mg twice daily (AI); or azithromycin 600 mg twice weekly (BIII) | Rifabutin 300 mg daily (dose adjusted based on concomitant ART) (BI); rule out active TB before starting |
| Streptococcus pneumoniae infection | Individuals who have not received any pneumococcal vaccine, regardless of CD4 count | 13-valent pneumococcal conjugate vaccine (PCV13) 0.5 mL IM (AI), followed in eight weeks by PPV23 if CD4 count ≥ 200 cells/mcL | 23-valent pneumococcal polysaccharide vaccine (PPV23) 0.5 mL IM (BII). For individuals who have previously received PPV23, one dose of PCV13 should be given at least one year after the last receipt of PPV23 (AII). |
| Re-vaccination is recommended for patients 19 to 64 years of age and ≥5 years since the first PPV23 dose; or ≥65 years of age and ≥5 years since the previous PPV23 dose. | PPV23 0.5 mL IM or SQ (BIII) | — | |
| Influenza A and B virus infection | All HIV-infected patients (AIII) | Inactivated influenza vaccine annually (AIII) | Note: Live-attenuated influenza vaccine is contraindicated in HIV-infected patients (AIII). |
| Syphilis | Persons who have had sexual contact with a person who receives a diagnosis of primary, secondary, or early latent syphilis within 90 days preceding the diagnosis, even if serologic test results are negative (AIII), or who have had sexual contact with a person who receives a diagnosis of primary, secondary, or early latent syphilis >90 days before the diagnosis should be treated presumptively for early syphilis if serologic test results are not immediately available and the opportunity for follow-up is uncertain (AIII). | Benzathine penicillin G 2.4 million units IM for 1 dose (AII) | For penicillin-allergic patients: doxycycline 100 mg twice daily for 14 days (BII); or ceftriaxone 1 g IM or IV daily for 8–10 days (BII); or azithromycin 2 g for 1 dose (BII) (not recommended for MSM or pregnant women [AII]) |
| Histoplasma capsulatum infection | CD4 count <150 cells/mcL and at high risk because of occupational exposure or living in a community with a hyperendemic rate of histoplasmosis (>10 cases/100 patient-years) (BI) | Itraconazole 200 mg daily (BI) | — |
| Coccidioidomycosis | A new positive IgM or IgG serologic test in patients who live in a disease-endemic area and with CD4 count <250 cells/mcL (BIII) | Fluconazole 400 mg daily (BII) or itraconazole 200 mg twice daily (BII) | Voriconazole 200 mg twice daily after a loading dose of 400 mg twice on first day; or posaconazole (delayed-release tablet) 300 mg daily; or posaconazole (oral suspension) 400 mg twice daily |
| Varicella-zoster virus (VZV) infection (pre-exposure) | Patients with CD4 counts ≥200 cells/mcL who have not been vaccinated, have no history of varicella or herpes zoster, or who are seronegative for VZV (CIII); vaccination not recommended for patients with CD4 counts <200 cells/mcL (AIII) | Primary varicella vaccination (Varivax), 2 doses (0.5 mL SQ each) administered three months apart (CIII). | VZV-susceptible household contacts of susceptible HIV-infected persons should be vaccinated to prevent potential transmission of VZV to their HIV-infected contacts (BIII). |
| Varicella-zoster virus (VZV) infection (post-exposure) | Close contact with a person with chickenpox or herpes zoster and is susceptible (i.e., no history of vaccination or of either condition or known to be VZV seronegative) (AIII) | Varicella-zoster immune globulin (VariZIG) 125 IU IM per 10 kg (maximum: 625 IU), administered as soon as possible and within 10 days after exposure (AIII) | Acyclovir 800 mg five times per day for 5–7 days (BIII); or valacyclovir 1 g three times per day for 5–7 days (BIII) |
| Human papillomavirus (HPV) infection | Age 11 to 26 years (BIII) | HPV 9-valent vaccine 0.5 mL IM at months 0,1–2, and 6 for men and women (BIII); patients that have completed the recombinant bivalent or quadrivalent vaccine series should receive the 9-valent vaccine as it protects against additional strains (CIII) | — |
| Hepatitis B virus (HBV) infection | Patients without chronic HBV or without immunity to HBV (i.e., anti-HBs <10 IU/mL) (AII); or patients with isolated anti-HBc and negative HBV DNA (BII). Early vaccination is recommended before CD4 count falls below 350 cells/mcL (AII). However, in patients with low CD4 cell counts, vaccination should not be deferred until CD4 count reaches >350 cells/mcL, because some patients with CD4 counts <200 cells/mcL do respond to vaccination (AII). | HBV vaccine IM (Engerix-B 20 mcg/mL or Recombivax HB 10 mcg/mL) at 0, 1, and 6 months (AII); HBV vaccine IM (Engerix-B 40 mcg/mL or Recombivax HB 20 mcg/mL), 0, 1, 2 and 6 months (BI); or combined HAV and HBV vaccine (Twinrix) 1 mL IM as a 3-dose (0, 1, and 6 months) or 4-dose (days 0, 7, 21 to 30, and 12 months) series (AII) | Some experts recommend vaccinating with 40-mcg doses of either recombinant HBV vaccine (CIII); some experts recommend a 4-dose schedule (BI). Data for a two-dose hepatitis B vaccine conjugated to a TLR9 agonist (Heplisav-B) are lacking in patients with HIV, but it is an option with a CIII recommendation. (In four randomized controlled trials, Heplisav-B was superior to 3 doses of recombinant vaccine in HIV-negative persons.) |
| Vaccine non-responders: anti-HBs <10 IU/mL 1 month after vaccination series | Re-vaccinate with a second vaccine series (BIII) | HBV vaccine IM (Engerix-B 40 mcg/mL or Recombivax HB 20 mcg/mL), 0, 1, 2 and 6 months (BI) | |
| Malaria | Travel to disease-endemic area | Recommendations are the same for HIV-infected and HIV-uninfected patients. | — |
| Penicillium marneffei | Patients with CD4 cell counts <100 cells/mcL who live or stay for a long period in rural areas in northern Thailand, Vietnam, or Southern China (BI) | Itraconazole 200 mg once daily (BI) | Fluconazole 400 mg once weekly (BII) |
| aAll medications are taken orally unless otherwise indicated. | |||
| A) | the leading cause of death. | ||
| B) | the fifth leading cause of death. | ||
| C) | the twentieth leading cause of death. | ||
| D) | not a significant cause of mortality. |
AIDS is no longer a leading cause of death in women overall in the United States, but it remains the fifth leading cause of death in African American women 35 to 44 years of age [55]. Women of color have been disproportionately affected by HIV/AIDS, with Black women accounting for 64% of new HIV diagnoses among women in the United States while representing only 13% of the female population [53]. Women of color also tend to contract HIV at a younger age than their White counterparts.
| A) | Cervical cancer | ||
| B) | Oral hairy leukoplakia | ||
| C) | Recurrent vulvovaginal candidiasis | ||
| D) | Human papillomavirus-related cervical dysplasia |
Gender-specific manifestations of HIV disease include irregular menstruation, recurrent vulvovaginal candidiasis, human papillomavirus (HPV)-related cervical dysplasia (abnormal, precancerous cell growth), and cervical cancer [59]. HIV-infected women have a higher prevalence of HPV infection, a higher risk of progression from infection to disease, and an increased risk of invasive cervical cancer and other HPV-related cancers than non-infected women [59]. Research indicates that cART does not significantly decrease the incidence of HPV-related cancers. As such, the American College of Obstetricians and Gynecologists recommends that women with HIV should have cervical cytology screening twice in the first year after diagnosis and annually thereafter [60].
| A) | within one to two weeks of initiation of therapy, then every three to four months. | ||
| B) | within one to two months of initiation of therapy, then every six to eight months. | ||
| C) | after six months of initiation of therapy, then annually thereafter. | ||
| D) | after one year of proven adherence to therapy. |
As with adults, cART is believed to play a major role in slowing progression of HIV in children and adolescents. Children receiving cART should be monitored for side effects, adherence, efficacy and toxicity. Recommendations for initial antiretroviral therapy of HIV infection in children have been updated based on FDA approvals and new data; clinicians should consult Department of Health and Human Services Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection when making management decisions for pediatric HIV care [67]. Following initiation of cART, all pediatric patients should be evaluated within one to two weeks to monitor compliance, side effects, and response to treatment. Subsequent visits should be scheduled every three to four months [67]. Strategies to improve adherence should focus on selecting an appropriate regimen, educating the family/caregiver, and consistent follow-up.
| A) | Less than 1% | ||
| B) | 9% | ||
| C) | 17% | ||
| D) | 44% |
Approximately 17% of newly diagnosed cases of HIV in 2018 occurred in individuals 50 years of age or older; 51% of all persons living with HIV/AIDS are 50 years of age or older [68]. Until recently, there had been little attention given to this group. HIV/AIDS has traditionally been thought to be the disease of the young; therefore, in the past, prevention and education campaigns had not been targeted toward older adults. However, evidence points to the increasing number of infected older people and a need for change in prevention and education campaigns. Some older persons may have less knowledge about HIV and risk reduction strategies. Due to divorce or being widowed and the availability of medications to treat erectile dysfunction, increasing numbers of older people are becoming sexually active with multiple partners [68]. For postmenopausal women, contraception is no longer a concern, and they are less likely to use a condom. Furthermore, vaginal drying and thinning associated with aging can result in small tears or cuts during sexual activity, which also raises the risk for infection with HIV/AIDS [68]. Studies indicate that at-risk individuals in this age group are significantly less likely than younger at-risk adults to use condoms during sex [69]. In addition, healthcare professionals are less likely to discuss sexual activity or take a sexual history if the patient is older than 50 years of age [69]. The combination of these factors increases the risk for unprotected sex with new or multiple partners in this age group, thereby increasing their risk for AIDS. This increase should be considered when evaluating older patients.
| A) | Persons who have injected drugs not prescribed by a clinician in the past six months who have also shared injection or drug preparation equipment in the past six months | ||
| B) | A heterosexual adult who has had sex with an opposite-sex partner in the past six months and is in an ongoing sexual relationship with an HIV-positive partner | ||
| C) | An MSM who has had a male sex partner in the past six months, is not in a monogamous partnership with a recently tested, HIV-negative man, and was diagnosed with gonorrhea three months ago | ||
| D) | All of the above |
In 2021, the CDC and the U.S. Department of Health and Human Services updated their clinical practice guidelines for pre-exposure prophylaxis for the prevention of HIV infection [72]. This guideline outlines indications for prophylaxis as one prevention option for HIV transmission. The most important first step in determining if an individual is a candidate for pre-exposure prophylaxis is a thorough history, including sexual and injection drug activities. All candidates will be adults without an acute or established HIV diagnosis. Pre-exposure prophylaxis is indicated for high-risk MSM, meaning those who have had any male sex partners in the past six months, are not in a monogamous partnership with a recently tested, HIV-negative man, and have one of the following [72]:
Anal sex without condoms (receptive or insertive) in the past six months
Any STI diagnosed or reported in the past six months
An ongoing sexual relationship with an HIV-positive man
Prophylaxis is also recommended for high-risk heterosexual adults who have had sex with an opposite sex partner(s) in the past six months, are not in a monogamous partnership with a recently tested, HIV-negative partner, and one of the following [72]:
Is a man who has sex with both women and men (behaviorally bisexual)
Infrequently uses condoms during sex with one or more partners of unknown HIV status who are known to be at substantial risk of HIV infection (IDU or bisexual male partner)
Is in an ongoing sexual relationship with an HIV-positive partner
IDUs are also considered candidates for pre-exposure prophylaxis if they meet certain criteria. The guideline states that persons who have injected drugs not prescribed by a clinician in the past six months may be candidates for prophylaxis if they also are positive for one of the following factors [72]:
Any sharing of injection or drug preparation equipment in the past six months
Increased risk of sexual acquisition (based on the previously outlined criteria)
| A) | 52.1% | ||
| B) | 66.3% | ||
| C) | 85.3% | ||
| D) | 96.7% |
Many adolescents engage in behaviors that put them at risk for HIV infection. According to the CDC, 39.5% of high school students [76]. Approximately 45.7% of currently sexually active high school students had not used a condom at last sexual intercourse; 1.6% had ever injected an illegal drug [76]. Although 85.3% of adolescents report having received education on HIV prevention in school, the content of these discussions may not provide adequate information on the subject. Furthermore, the American Academy of Pediatrics determined that school-based education and intervention programs do not provide the necessary opportunities of confidential discussions or targeted counseling [77]. Healthcare professionals have a unique opportunity to intervene in this population to provide accurate and complete information on HIV transmission and risk reduction.