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reduces morbidity and improves prognosis and thus increases the likelihood of a fit assessment.
Note 2.— Guidance on the assessment of applicants who are seropositive for human
immunodeficiency virus (HIV) is contained in the Manual of Civil Aviation Medicine (Doc 8984).
The main purpose of the guidance material contained in this section is to assist with determining the
requirements for a full investigation and risk assessment for disease that might lead to incapacitation in
HIV-seropositive applicants.
BACKGROUND
HIV infection is pandemic with cases reported from virtually every country in the world. Untreated the
infection usually leads to Acquired Immunodeficiency Syndrome (AIDS) with AIDS-defining
opportunistic infections or associated illnesses. A 2007 report from UNAIDS/WHO estimated that 33.2
million people are living with HIV. There were 2.5 million new infections in 2007 with 1.7 million (68
per cent) of these occurring in sub-Saharan Africa and important increases in Eastern Europe and central
Asia, where there are some indications that infection rates have risen by more than 50 per cent since 2004.
In 2006, 2.1 million people died of AIDS-defining illnesses. The prevalence of HIV infection in pilots
and air traffic controllers is unknown.
CAUSATIVE AGENT
In 1984, the human immunodeficiency virus type 1 (HIV-1) was discovered as the primary causative
agent of AIDS. In 1986, a second type of HIV, called HIV-2, was isolated from AIDS patients from West
Africa. Both HIV-1 and HIV-2 have the same modes of transmission and are associated with similar
opportunistic infections and AIDS. In persons infected with HIV-2, immunodeficiency seems to develop
more slowly and to be milder. HIV-2 infection is predominantly found in West Africa and there is less
known about managing HIV-2 infection and predicting outcomes, than for HIV-1. Care is required,
therefore, when interpreting the information provided in this chapter to determine fitness for certification
of persons with HIV-2 infection.
The aetiological agent is a retrovirus and the CD4+ T-lymphocyte is the primary target for HIV infection.
The CD4+ T-lymphocyte coordinates a number of important immunological functions, and a loss of these
ICAO Preliminary Unedited Version — November 2009 III-13-2
functions results in progressive impairment of the immune response. Studies of the natural history of HIV
infection have documented a wide spectrum of disease manifestations, ranging from asymptomatic
infection to life-threatening conditions characterized by severe immunodeficiency, serious opportunistic
infections, and cancers. Other studies have shown a strong association between a decrease of the number
of CD4+ T-lymphocytes and an increase of the risk and severity of opportunistic illnesses.
TRANSMISSION
HIV is transmitted by sexual contact (both homosexual and heterosexual), by blood and blood products,
and by infected mothers to infants either intrapartum, perinatally, or via breast milk. There is no evidence
that HIV is transmitted by casual contact or by insects, such as mosquito bites. HIV has been
demonstrated in seminal fluid, cervical smears, and vaginal fluid. In these it appears to concentrate where
there are increased numbers of lymphocytes and monocytes in the fluid, as in genital inflammatory
conditions. There are strong associations of HIV transmission with a history of sexually transmitted
diseases (STDs) and of HIV transmission with anal intercourse. Although the virus can be identified from
virtually any body fluid, there is no evidence that transmission can occur via exposure to tears, sweat, and
urine. There is no convincing evidence that saliva can easily transmit HIV infection, although occasional
cases have been reported in which the victim was bitten by someone infected with HIV.
COURSE OF HIV INFECTION
The typical course of the HIV-infection in untreated patients is presented in Figure 1. After entrance of
the virus in the host system, the CD4+ T cells (and to lesser extent cells of monocyte lineage) are the
major targets of HIV infection.
In primary HIV infection, virus replication
in CD4+ T cells intensifies prior to the
initiation of an HIV-specific immune
response, leading to a burst of viraemia and
to rapid dissemination of virus to other
lymphoid organs, brain, and other tissues. At
that stage, 3-6 weeks after primary infection,
50-70 per cent of the patients experience an
“acute retroviral syndrome” (acute HIV
infection). The hallmark of acute infection is
a high level HIV ribonucleic acid (RNA) or
viral p24 antigen in conjunction with a
negative HIV enzyme-linked immunosorbent
assay (ELISA) test, negative or
　
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