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NAME: Human immunodeficiency virus (HIV).

SYNONYM OR CROSS REFERENCE: HIV, acquired immune deficiency syndrome, AIDSFootnote 1-Footnote 20. Was previously known as lymphadenopathy-associated virus, human T-lymphotropic virus type III (HTLV-III), immunodeficiency-associated virus, and AIDS-associated retrovirusFootnote 1-Footnote 20.

CHARACTERISTICS: HIV is a member of the Retroviridae family, genus LentivirusFootnote 14,Footnote 16. HIV is an icosahedral, enveloped virus, of approximately 100 to 110 nm in diameter, and has a single-stranded, linear, positive-sense RNA genomeFootnote 14,Footnote 16. HIV has two recognised strains: HIV-1 and HIV-2Footnote 11,Footnote 16,Footnote 17. Upon entry into the host cell, retroviral RNA is converted to DNA by a virally encoded reverse transcriptase enzyme, the DNA transcript is integrated into the host’s chromosomal DNAFootnote 14.


PATHOGENICITY/TOXICITY: AIDS is characterised by symptoms and infections caused by the breakdown of the immune system (by destruction or functional impairment of CD4 receptors) due to HIV infectionFootnote 10,Footnote 12. HIV can infect many cell types, mainly lymphocytes, but also macrophages, and microglia in the brain, and other neurological cells, resulting in profound asthenia, dementia and damage to the peripheral nervous systemFootnote 12. Due to immunodeficiency, patients succumb to various fungi, parasites, bacteria, and/or viruses and are prone to certain tumoursFootnote 10,Footnote 12. Globally, Mycobacterium tuberculosis is the most common cause of death of HIV-infected individuals. The clinical features of HIV infection vary depending on the stage of the diseaseFootnote 6. Acute infection is accompanied by non-specific “flu-like” and “mononucleosis-like” symptoms such as myalgia, arthralgia, diarrhoea, nausea, vomiting, headache, hepatosplenomegaly, weight loss, and neurological symptomsFootnote 6,Footnote 16,Footnote 21. Early-stage disease refers to the period of clinical latency between the time of the primary infection and the development of symptoms indicative of advanced immunodeficiency. Typically, when the patient’s CD4+ T-cell count falls below 500 cells/µL, syndromes indicative of depressed cell mediated immunity can appear. Examples include orophayngeal and recurrent vulvovaginal candidiasis, bacillary angiomatosis, recurrent or multidermatomal herpes zoster, listeriosis, infections due to Rhodococcus equi, pelvic inflammatory disease, oral hairy leukoplakia associated with Epstein-Barr virus, cervical dysplasia, long lasting diarrhoea, idiopathic thrombocytopenic purpura, and peripheral neuropathyFootnote 21. Late-stage disease refers to the period when the patient’s CD4+ T-cell count falls below 200 cells/µLFootnote 10,Footnote 21. The loss of the integrity of cell-mediated immune responses allows ubiquitous environmental organisms with limited virulence to become life threatening pathogensFootnote 6. Examples of conditions (as set out by the US Centers for Disease Control and Prevention) include candidiasis of bronchi, trachea, lungs or oesophagus, invasive cervical cancer, coccidioidomycosis, cryptococcosis, cryptosporidiosis, cytomegalovirus disease (other than liver, spleen, or nodes), cytomegalovirus retinitis (with loss of vision), HIV-related encephalopathy, herpes simplex, histoplasmosis, isosporiasis, Kaposi’s sarcoma, Burkitt’s lymphoma, immunoblastic lymphoma, primary lymphoma of the brain, Mycobacterium avium complex, Mycobacterium tuberculosis, Pneumocystis jirovecii pneumonia, recurrent pneumonia, progressive multifocal leukoencephalopathy, recurrent salmonella septicaemia, toxoplasmosis of the brain, and wasting syndrome due to HIVFootnote 21.

EPIDEMIOLOGY: HIV is a major global problem with approximately 25 million HIV-related deaths and another 40.3 (36 to 45.3) million infected individuals worldwideFootnote 17. AIDS was first described in 1981. The new retrovirus (HIV-1) was found in tissues from AIDS patients in 1983 and the causative relationship between HIV and AIDS was established in 1984Footnote 3,Footnote 12. HIV-2 was discovered in 1986 and is the least pathogenic form of HIV, displaying low rates of transmission and rarely causing AIDSFootnote 4. The majority of people with HIV live in the developing world (approximately 95% of the individuals infected worldwide). Sub-Saharan Africa is by far the worst-affected area in the worldFootnote 10. This region has slightly more than 10% of the world’s population but is home to more than 60% of the total population living with HIV/AIDSFootnote 10.

Globally, infants who acquire the disease from their mothers constitute about 11% of all HIV infectionsFootnote 10. Ten percent of infections worldwide are associated with injection drug use; 5 to 10% are transmitted by sex between men; and 5 to 10% occur in health care settingsFootnote 10. The predominant means of infection is sex between men and women, which accounts for nearly two thirds of new infections, and 85% of existing infections worldwideFootnote 10,Footnote 17. About 50% of all new HIV infections worldwide occur in individuals younger than 25 years oldFootnote 10.

HOST RANGE: HumansFootnote 3-Footnote 6,Footnote 8,Footnote 10-Footnote 13,Footnote 15-Footnote 17,Footnote 20-Footnote 23.


MODES OF TRANSMISSION: HIV is transmitted either by exposure of the virus to oral, rectal, or vaginal mucosa during sexual activity; by intravascular inoculation through transfusion of contaminated blood products; by using contaminated equipment during injection drug use; or from mother to infant during pregnancy, delivery or breastfeedingFootnote 6,Footnote 16. There are no obvious differences in disease manifestations in individuals infected by mucosal versus blood-borne routesFootnote 6. Sexual transmission accounts for more than 90% of HIV infections worldwideFootnote 6,Footnote 16.

INCUBATION PERIOD: Variable. Commonly the time from infection to the development of detectable antibodies is generally 1 to 3 months; however, the time from HIV infection to diagnosis of AIDS had an observed range of less than 1 year to 15 years or longerFootnote 11.

COMMUNICABILITY: The highest levels of per-act risk for HIV transmission from person-to-person are: blood transfusion from an infected donor, needle sharing by infected injection-drug users, receptive anal intercourse, and percutaneous needle injuriesFootnote 6,Footnote 11,Footnote 12,Footnote 20. Insertive anal intercourse, penile-vaginal exposures, and oral sex represent substantially less per-act riskFootnote 6,Footnote 11,Footnote 20. HIV can also be passed from mother to child in utero (vertical) as well as during childbirth, and from breast milkFootnote 6,Footnote 11. HIV has also been documented to have been transmitted by bite injuriesFootnote 22.The period of communicability begins early after HIV infection and is thought to last throughout the life of the infected individualFootnote 11. Infectiousness is related to viral load.


RESERVOIR: HumansFootnote 6,Footnote 8,Footnote 10-Footnote 12,Footnote 16,Footnote 17,Footnote 22.

ZOONOSIS: None, although current evidence suggests that HIV-1 and HIV-2 entered into the human population through multiple zoonotic infections from simian immunodeficiency virus-infected non-human primatesFootnote 17.

VECTORS: No laboratory or epidemiological evidence suggests that biting insects have transmitted HIV infectionFootnote 11,Footnote 16.


DRUG SUSCEPTIBILITY: Antiretroviral agents from 5 drug classes are currently available to treat HIV infection, namely: the nucleoside reverse transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors (NtRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), proteinase inhibitors (PIs), and fusion inhibitorsFootnote 10,Footnote 15.

SUSCEPTIBILITY TO DISINFECTANTS: HIV is susceptible to fresh 2% glutaraldehyde, 2% Jodopax (detergent and iodine), hypochlorite, iodine, phenolics, and to a lesser extent 70% ethanol, NaOH and isopropanolFootnote 7,Footnote 9,Footnote 18.

PHYSICAL INACTIVATION: HIV is inactivated by ultraviolet (UV) light; however, the level of the inactivation is heavily influenced by the proximity of the UV source to the sample and the concentration of protein in the sample environment. HIV is easily inactivated in a cell free medium; however, in cell associated samples and blood samples complete inactivation requires much longer exposures to the UV sourceFootnote 7. HIV is also inactivated at pH higher or lower than the optimal level of 7.1Footnote 18. A temperature of 60°C for 30 minutes will likely inactivate HIV; however, higher temperatures and incubations may be required depending on the initial titre of the virusFootnote 18.

SURVIVAL OUTSIDE HOST: HIV can remain viable in blood in syringes at room temperature for 42 days, and in blood and cerebrospinal fluid from autopsies for up to 11 daysFootnote 1,Footnote 2. Although drying in the environment is known to cause a rapid reduction in HIV concentration, under experimental conditions, Cell-free HIV dried onto a glass coverslip in 10% serum can survive for longer than 7 days, depending on the initial titreFootnote 19.


SURVEILLANCE: HIV is diagnosed by tests that assess whether an individual’s immune system has produced an HIV-specific immune responseFootnote 16. Common tests include the indirect binding assay, antibody capture assay, the double antigen sandwich, ELISA, immunofluorescence, Western blotting, line immunoassays, and PCR, as well as viral isolationFootnote 16.

FIRST AID/TREATMENT: AIDS must be managed as a chronic disease. Antiretroviral treatment is complex, involving a combination of drugs and resistance will appear rapidly if only a single drug is usedFootnote 11. The 5 available classes of antiretroviral drugs, NRTIs, NtRTIs, NNRTIs, PIs and fusion inhibitors, can be combined to provide highly active antiretroviral therapy (HAART). For many (but not all) patients, HAART converts an inexorably fatal disease into a chronic disease with a fairly good prognosisFootnote 8,Footnote 13.


PROPHYLAXIS: HIV postexposure prophylaxis regimens are based on the nature of the exposure. The majority of HIV exposures will warrant a two drug regimen, using 2 NRTIs or 1 NRTI and 1 NtRTI. Combinations include: zidovudine (ZDV) and lamivudine (3CT) or emtricitabine (FTC); stavudine (d4T) and 3TC or FTC; and tenofovir (TDF) and 3TC or FTCFootnote 15.

The addition of a third or fourth drug should be considered for exposures that pose an increased risk of transmission. The preferred drugs in this case are proteinase inhibitors such as lopinavir/ritonavir (LPV/RTV)Footnote 15,Footnote 16.


LABORATORY-ACQUIRED INFECTIONS: Although there have been many reported cases of HIV infection through occupational transmission, the numbers of laboratory acquired infections are low. As of 2001, there have been a total of 57 cases of documented occupationally acquired HIV among U.S. health care workersFootnote 24.

SOURCES/SPECIMENS: Blood, semen, vaginal secretions, cerebrospinal fluid, synovial fluid, peritoneal fluid, pleural fluid, pericardial fluid, amniotic fluid, other specimens containing visible blood, breast milk, unscreened or inadequately treated blood products, and infected human tissuesFootnote 11,Footnote 15,Footnote 16.

Faeces, nasal secretions, sputum, sweat, vomitus, saliva, tears, and urine, are not considered potentially infectious unless they are visibly bloodyFootnote 11,Footnote 15.

PRIMARY HAZARDS: Needlestick, contaminated sharp objects, and/or direct contact of non-intact skin or mucous membranes with HIV-infected specimens/tissuesFootnote 15,Footnote 16.

SPECIAL HAZARDS: Extreme care must be taken to avoid spilling and/or splashing infected materials. HIV should be presumed to be in/on all equipment and devices coming in direct contact with infected materialsFootnote 25.



CONTAINMENT REQUIREMENTS: Please refer to the Biosafety Directive for Human Immunodeficiency Virus (HIV) and Human T-cell Lymphotropic Virus Type 1 (HTLV-1).

PROTECTIVE CLOTHING: Solid-front gowns with tight-fitting wrists, gloves, and respiratory protection should be worn over laboratory clothing when infectious materials are directly handledFootnote 25.

OTHER PRECAUTIONS: All activities with infectious material should be conducted in a biological safety cabinet (BSC) or other appropriate primary containment device in combination with personal protective equipment. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are unloaded in a biological safety cabinet. The use of needles, syringes, and other sharp objects should be strictly limited. Open wounds, cuts, scratches, and grazes should be covered with waterproof dressings. Additional precautions should be considered with work involving animals or large scale activitiesFootnote 25.


SPILLS: Allow aerosols to settle and, while wearing protective clothing, gently cover the spill with paper towels and apply 1% sodium hypochlorite starting at the perimeter, working inwards towards the centre. Allow sufficient contact time before clean upFootnote 25.

DISPOSAL: Decontaminate all materials for disposal by steam sterilisation, chemical disinfection, and/or incinerationFootnote 25.

STORAGE: Infectious material should be stored in sealed, leak-proof containers that are appropriately labelledFootnote 25.


REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: September 2016.

PREPARED BY: Centre for Biosecurity, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Material Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.


Public Health Agency of Canada, 2016



Footnote 1
Abdala, N., Reyes, R., Carney, J. M., & Heimer, R. (2000). Survival of HIV-1 in syringes: Effects of temperature during storage. Substance use and Misuse, 35(10), 1369-1383.
Footnote 2
Ball, J., Desselberger, U., & Whitwell, H. (1991). Long-lasting viability of HIV after patient's death [30]. Lancet, 338(8758), 63.
Footnote 3
Barre Sinoussi, F., Chermann, J. C., & Rey, F. (1983). Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS). Science, 220(4599), 868-871.
Footnote 4
Clavel, F., Guétard, D., Brun-Vézinet, F., Chamaret, S., Rey, M., Santos-Ferreira, M. O., Laurent, A. G., Dauguet, C., Katlama, C., Rouzioux, C., Klatzmann, D., Champalimaud, J. L., & Montagnier, L. (1986). Isolation of a new human retrovirus from West African patients with AIDS. Science, 233(4761), 343-346.
Footnote 5
Coffin, J., Haase, A., Levy, J. A., Montagnier, L., Oroszlan, S., Teich, N., Temin, H., Toyoshima, K., Varmus, H., & Vogt, P. (1986). What to call the AIDS virus? Nature, 321(6065), 10.
Footnote 6
Cohen, O. J., & Fauci, A. S. (2001). Pathogenesis and Medical Aspects of HIV-1 infection. In D. M. Knipe, & P. M. Howley (Eds.), Fields Virology (pp. 2043-2094). Philadelphia, PA.: Lippencott-Raven.
Footnote 7
Druce, J. D., Jardine, D., Locarnini, S. A., & Birch, C. J. (1995). Susceptibility of HIV to inactivation by disinfectants and ultraviolet light. Journal of Hospital Infection, 30(3), 167-180.
Footnote 8
Greene, W. C. (2007). A history of AIDS: Looking back to see ahead. European Journal of Immunology, 37(SUPPL. 1), S94-S102.
Footnote 9
Hansen, P. J. (1989). Chemical inactivation of HIV on surfaces. BMJ (Clinical Research Ed.), 299(6693), 260.
Footnote 10
Harris, A., & Bolus, N. E. (2008). HIV/AIDS: an update. Radiologic Technology, 79(3), 243-252; quiz 253-255.
Footnote 11
Heymann, D. L. (2004). An Official Report of the American Public Health Association. In D. L. Heymann (Ed.), Control of Communicable Diseases Manual. (18th ed., pp. 75-81). Washington, D.C.: American Public Health Association.
Footnote 12
Kallings, L. O. (2008). The first postmodern pandemic: 25 Years of HIV/AIDS. Journal of Internal Medicine, 263(3), 218-243.
Footnote 13
Kempen, J. H. (2008). Medical management of human immunodeficiency virus infection. Indian Journal of Ophthalmology, 56(5), 385-390.
Footnote 14
Knipe, D. M., & Howley, P. M. (Eds.). (2001). Fields Virology (4th ed.). Philidelphia: Lippincot Williams & Wilkins.
Footnote 15
Panlilio, A. L., Cardo, D. M., Grohskopf, L. A., Heneine, W., & Ross, C. S. (2005). Updated U.S. Public Health Service guidelines for the management of occupational exposures to HIV and recommendations for postexposure prophylaxis. MMWR.Recommendations and Reports: Morbidity and Mortality Weekly Report.Recommendations and Reports / Centers for Disease Control, 54(RR-9), 1-17.
Footnote 16
Schupbach, J. (2003). Human Immunodeficiency virus. In P. R. Murray, E. J. Baron, J. H. Jorgensen, M. A. Pfaller & R. H. Yolken (Eds.), Manual of Clinical mircrobiology (8th ed., pp. 1253-1281). Washinton, DC: ASM press.
Footnote 17
Takebe, Y., Uenishi, R., & Li, X. (2008). Global Molecular Epidemiology of HIV: Understanding the Genesis of AIDS Pandemic
Footnote 18
Tjotta, E., Hungnes, O., & Grinde, B. (1991). Survival of HIV-1 activity after disinfection, temperature and pH changes, or drying. Journal of Medical Virology, 35(4), 223-227.
Footnote 19
Van Bueren, J., Simpson, R. A., Jacobs, P., & Cookson, B. D. (1994). Survival of human immunodeficiency virus in suspension and dried onto surfaces. Journal of Clinical Microbiology, 32(2), 571-574.
Footnote 20
Varghese, B., Maher, J. E., Peterman, T. A., Branson, B. M., & Steketee, R. W. (2002). Reducing the risk of sexual HIV transmission: Quantifying the per-act risk for HIV on the basis of choice of partner, sex act, and condom use. Sexually Transmitted Diseases, 29(1), 38-43.
Footnote 21
1993 revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. (1992). MMWR.Recommendations and Reports: Morbidity and Mortality Weekly Report.Recommendations and Reports / Centers for Disease Control, 41(RR-17), 1-19.
Footnote 22
Vidmar, L., Poljak, M., Tomazic, J., Seme, K., & Klavs, I. (1996). Transmission of HIV-1 by human bite [2]. Lancet, 347(9017), 1762-1763.
Footnote 23
Collins, C. H., & Kennedy, D. A. (Eds.). (1983). Laboratory-acquired Infections (4th ed.). Oxford: Butterworth-Heinermann.
Footnote 24
Do, A. N., Ciesielski, C. A., Metler, R. P., Hammett, T. A., Li, J., & Fleming, P. L. (2003). Occupationally acquired human immunodeficiency virus (HIV) infection: national case surveillance data during 20 years of the HIV epidemic in the United States. Infection Control and Hospital Epidemiology: The Official Journal of the Society of Hospital Epidemiologists of America, 24(2), 86-96. doi:10.1086/502178
Footnote 25
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.
Footnote 26
Human Pathogens and Toxins Act. S.C. 2009, c. 24. Government of Canada, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009, (2009).