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Human Immunodeficiency Virus Screening
Screening donated blood for human immunodeficiency virus (HIV) is critical to maintaining a safe blood supply. HIV transmission by intravenous administration of infected blood products proved to be highly efficient and accordingly, shortly after HIV-1 discovery in 1983, donor deferral measures were initiated and, in 1985, the first test was licensed for donor screening. Donor deferral and testing has decreased blood transfusion transmission from ∼1:100 transfused products in 1982 in the San Francisco area, to current estimates of <1:2 million products nationwide.
While HIV is not the most common infection found in donated blood, it is, perhaps, the most serious and is likely to be distressing to a donor. Therefore, fairly extensive and supportive counseling must be available. Additionally, false reactive screening results must be communicated to donors as well as the possibility of reentry testing to resume donating blood.
Description
HIV is a lentivirus, which is a subgroup of the retrovirus family, and the causative agent of acquired immune deficiency syndrome (AIDS). Retroviruses are RNA viruses with the presence of viral particle–associated reverse transcriptase and a unique replication cycle. Virus particles attach to the cell membrane (in the case of HIV, CD 4+ lymphocytes), subsequently enter into the host cell, then the reverse transcriptase enzyme copy viral RNA into cDNA (complementary double-stranded DNA), where cDNA is then integrated into host cell’s genome. Subsequent transcription, processing, and translation of viral genes are mediated by host cell enzymes. Particles then bud from the plasma membrane and infect other cells. In addition, virus can spread by fusion of infected and uninfected cells or by replication of integrated viral DNA during mitosis or meiosis.
Infection
HIV infection can be transmitted through sexual contact, in utero or childbirth, breastfeeding, and parenteral exposure to blood. The CDC reported that in the United States in 2015, the highest incidence of new diagnosis was in African-Americans, males, age 20–29 years old and the most common risk identified was male-to-male sex. Rate per 100,000 of new infections among women is dropped from 7.3% in 2010 to 5.4% in 2015. In comparison, among men, rate dropped from 27.3% in 2010 to 24.4% in 2015 ( https://www.cdc.gov/hiv/library/reports/hiv-surveillance.html ).
60% of acute HIV infections result in nonspecific flulike illness with incubation period of 2–4 weeks. Acute infection resolves in weeks to few months resulting in asymptomatic period that may last years. Eventually, the virus can no longer be controlled, as helper CD 4+ (T4) lymphocytes are destroyed. This loss of CD 4+ lymphocytes results in development of opportunistic infections and direct viral effects on multiple organs; together resulting in death on average after 3 years once AIDS is diagnosed, if not treated. Post infection survival has improved with the advent of potent antiretroviral therapies. However, these medications do not eradicate HIV and have multiple side effects. Moreover, resistant viral strains have been known to develop, which adds to the difficulty of treatment.
HIV Types
HIV types 1 and 2 (HIV-1 and HIV-2) infections both cause AIDS. HIV-1 family is divided into main (M), outlier (O), and non-M, non-O (N) groups. Group M has 11 distinct subtypes or clades (A–K). In the United States, clade B is almost exclusively prevalent. The greatest genetic diversity exists in Central Africa. Group O is the most common in Cameroon and surrounding West African countries (where it represents 1%–2% of HIV infections). Group O infection in the United States is very rare and is usually found in African immigrants or their partners. Previous generations of HIV antibody and nucleic acid assays did not reliably detect group O, but current assays have added sensitivity to group O. HIV-2 is also rare in the United States with no reported cases of HIV-2 transfusion transmission in the United States.
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