**Human Immunodeficiency Virus Transmission**

### Goselle Obed Nanjul1, 2

*1School of Biological Sciences, Bangor University 2Applied Entomology and Parasitology Unit, Department of Zoology, University of Jos, 1UK 2Nigeria* 

#### **1. Introduction**

Human Immunodeficiency Virus (HIV) is the causative organism of AIDS which has become one of the greatest public health challenges faced by mankind. AIDS was first identified in 1981 in Los Angeles, USA. Two types of HIV exist presently- HIV-1 and HIV-2 (Alizon et al., 2010; Adoga et al., 2010). HIV-1 was first isolated in the early 1980s (Barre-Sinoussi et al., 1983) and linked as causative agent of AIDS (Gallo et al., 1984). HIV-2 which is similar to HIV-1 was later identified in the developing world (Clavel, 1987, Clavel et al., 1986), but found to be less virulent and can differ in its response to antiretroviral agents. HIV-1 is classified into three groups [M, N and O] based on the genetic diversity. Group M (major) has 10 subtypes (A-J), and Group O (outlier) represents a number of highly divergent strains (Carr et al., 1998; Jassens et al., 1997 Chen et al., 2010). Francois Simon and his group reported a group N of HIV-1. Despite the phenotypic classification of HIV-1 into subtypes, the number of sequenced isolates remains limited (Sharp et al., 1994). Both strains are spread in the same way and have the same AIDS causing consequences. While HIV-1 has been reported to have a shorter incubation period of 7-10years, HIV-2 is considerably longer and often less severe (Barre-Sinoussi, 1996; WHO, 1989).

HIV infection is usually followed by a chronic progressive destruction of the immune and neurologic system (Price, 1996), which if not managed leads to the possible invasion and establishment of multiple opportunistic infections.( Lindo et al., 1998; Pozio et al., 1997) and malignancy (Schulz et al., 1996). Although on average, an infected individual spends several years without manifesting the disease, AIDS has always been certain. The time from infection to AIDS varies widely between individuals, from a few months to as many as 20 years with existing evidences accepting that 50% of individuals progress to AIDS in 7-10years and this has been accepted as the incubation period of the virus (Del Amo et al., 1998; WHO, 1994).

#### **2. Portals of HIV transmission**

The concentration of virus in a body fluid and the extent of exposure to body fluids determine to a great extent the transmission of a virus. Jaffe and McMahon-Pratt (1983) first indicated in their Epidemiological studies conducted in 1981 and 1982 that the major channel of transmission of AIDS were intimate sexual contact and contaminated blood. Gottlieb et al (1981); Masur et al (1981); Siegal et al (1981); Callazos et al (2010); van

Human Immunodeficiency Virus Transmission 45

For conveniences, we will share the mode of infections into: Sexual and Non-sexual.

Fig. 2. Routes of Transmission of Human Immuno-deficiency Virus. [HIV]

Fig. 3. Levels of HIV load in semen [Courtesy:…]

Low HIV plasma load,

but high semen load

Testis

Griensven and de Lin van Wijngaarden (2010) all described the syndrome in homosexual and bisexual men and, intravenous drug users, while Harris et al (1983); Padian et al (1991); Cameron et al (1989); Quinn et al (2000) and Decker et al (2010) recognised their mode of transmission through heterosexual activity. Evidences later showed that transmission recipients and haemophiliacs could contract the illness from blood or blood products (CDC, 1982; Peterson, 1992; CDC, 2010) and newborn infants get infected from their mothers' (Ammann et al., 1983; Scarlatti, 1996; Brookmeyer, 1991; Landesman, et al., 1996; Goedert et al., 1989; Mackelprang et al., 2010). Brookmeyer (1991); Stoneburner et al (1990) all agreed that the three principal means of transmission – blood, sexual contact and mother-to-child have not changed which could be attributed to a greater degree to the relative amount of the virus in various body fluids.

Fig. 1. Diagrammatic representation of HIV-1 and HIV-2 showing their dependent and independence on CD4+ [Courtesy-]

HIV is present in semen (including pre-seminal fluid), vaginal/cervical secretions and blood, breast milk expressed through feeding; organ donations; sharing infected objects (needles, tattoos and piercing) which are the main vehicles through which the virus is transmitted (Kim et al., 2010; Yu et al., 2010; Suligoi et al., 2010; Pruss et al., 2010 and Baggaley et al., 2010). The virus may also be present in saliva, tears, urine, cerebrospinal fluid and infected discharges, but these are not vehicles of which HIV is spread. Epidemiological survey do not support transmission through water or food, sharing eating utensils, coughing or sneezing, vomiting, toilets, swimming pools, insect bites, shaking of hands or other casual contacts, hence there is no public health reason for discrimination and or restrictions.

A study of French hospital patients by Grabar et al (2009) found that approximately 0.5% of HIV-1 infected individuals retain high levels of CD4+ T-cells and a low or clinically undetectable viral load without anti-retroviral treatment. These individuals are classified as HIV controllers or long-term non-progressors.

Griensven and de Lin van Wijngaarden (2010) all described the syndrome in homosexual and bisexual men and, intravenous drug users, while Harris et al (1983); Padian et al (1991); Cameron et al (1989); Quinn et al (2000) and Decker et al (2010) recognised their mode of transmission through heterosexual activity. Evidences later showed that transmission recipients and haemophiliacs could contract the illness from blood or blood products (CDC, 1982; Peterson, 1992; CDC, 2010) and newborn infants get infected from their mothers' (Ammann et al., 1983; Scarlatti, 1996; Brookmeyer, 1991; Landesman, et al., 1996; Goedert et al., 1989; Mackelprang et al., 2010). Brookmeyer (1991); Stoneburner et al (1990) all agreed that the three principal means of transmission – blood, sexual contact and mother-to-child have not changed which could be attributed to a greater degree to the relative amount of

Fig. 1. Diagrammatic representation of HIV-1 and HIV-2 showing their dependent and

HIV is present in semen (including pre-seminal fluid), vaginal/cervical secretions and blood, breast milk expressed through feeding; organ donations; sharing infected objects (needles, tattoos and piercing) which are the main vehicles through which the virus is transmitted (Kim et al., 2010; Yu et al., 2010; Suligoi et al., 2010; Pruss et al., 2010 and Baggaley et al., 2010). The virus may also be present in saliva, tears, urine, cerebrospinal fluid and infected discharges, but these are not vehicles of which HIV is spread. Epidemiological survey do not support transmission through water or food, sharing eating utensils, coughing or sneezing, vomiting, toilets, swimming pools, insect bites, shaking of hands or other casual contacts, hence there is

A study of French hospital patients by Grabar et al (2009) found that approximately 0.5% of HIV-1 infected individuals retain high levels of CD4+ T-cells and a low or clinically undetectable viral load without anti-retroviral treatment. These individuals are classified as

the virus in various body fluids.

independence on CD4+ [Courtesy-]

no public health reason for discrimination and or restrictions.

HIV controllers or long-term non-progressors.

For conveniences, we will share the mode of infections into: Sexual and Non-sexual.

Fig. 2. Routes of Transmission of Human Immuno-deficiency Virus. [HIV]

Low HIV plasma load, but high semen load

Fig. 3. Levels of HIV load in semen [Courtesy:…]

Human Immunodeficiency Virus Transmission 47

Transcriptase Inhibitor (NNRTIs) and Fusion Inhibitor Enfuvirtide have no activity against HIV-2 and in the light of the current albeit limited data, zidovudine mono-therapy should not be used. These factors make it crucial that proper selection of and adherence to the first antiretroviral combination regimen is in place in order to achieve a successful treatment response. Though of recent, a combination of Combivir and nevarapine is given to mothers to prevent transmission of HIV to children. The Emergency Lower Segment Caesarian Section (ELSCS) could be planned at 38 weeks of gestation with regards to the mode of delivery if the viral load is undetectable or the mother is either symptomatic or has low CD4 cell count. HIV is present in breast milk and postnatal transmission via breastfeeding is an important component of MTCT in Sub-Saharan Africa (Kreiss, 1997). World-wide, an estimated one in three of vertical transmission may be due to breastfeeding with above 12months of age carrying higher risk (Bulterys et al., 1995). Kuhn and Stein (1997) demonstrated that under certain conditions prevailing in specific settings in developing countries, breast feeding for six months would be preferable to breast feeding beyond this age. Breastfeeding has been reported to account for 5-15% of infants becoming infected with HIV-1 after delivery (ECS 1991; Ryder et al., 1989; Mok et al., 1989). Although the placental entry of some infections is a critical aspect of these infections, the role of placental cells and the mechanism by which pathogens pass from the maternal to the foetal circulation varies. The placenta provides a barrier that prevents transmission of some viruses, but allows others to reach the foetal circulation. Mother to foetus placental transmission of some viruses occurs through transcytosis across placental cells. The placenta may also act as a reservoir in which virus replicates before reaching the foetus. Placental transmission of HIV-1 is a complex incompletely understood process which requires advanced studies (Al-husaini, 2009). The antiretroviral therapy, zidovudine (ZDV) is metabolized into its active form in the placenta (Qian et al., 1994). ZDV inhibits HIV replication within placental cells. To reach the foetal circulation, HIV-1 should cross the trophoblastic placental barrier (cytotrophoblasts and syncitiotrophoblasts). Blood borne maternal pathogens that arrive at the uteroplacental circulation and intervillous space may reach the foetus through the villous capillaries. HIV-1 has been detected on both the maternal and the foetal parts of the placenta. HIV-1 experiences replication in the placenta. The virus may cross the trophoblastic barrier by endocytosis, or by an injured villous surface. However, superficial breaks in syncytiotrophoblast cells do not radically affect the vertical transmission of viruses (Burton et al., 1996). The reverse transcriptase enzyme of HIV-1 is important in the life cycle of the virus by converting the single-stranded RNA genome into double-stranded DNA that integrates into the host chromosome. There is a lower degree of viral heterogeneity in transmitting mothers compared

with nontransmitting mothers (Sundaravaradan et al., 2005).

of vertical transmission (Al-husaini, 2009).

years earlier)[UNAIDS, 2010].

Human chorionic gonadotropin (hCG) has been shown in vitro to inhibit reverse transcriptase and to block viral transmission between virus-carrying lymphocytes and placental trophoblasts (Bourinbaiar and Lee-Huang, 1995). However, role of hCG in protecting the foetus from vertical transmission HIV-1 needs to be studied. In summary, the restricted heterogeneity of HIV-1 in the infected mothers is more likely associated with lack

As access to services for preventing the mother-to-child transmission of HIV has increased, the total number of children being born with HIV has also decreased. An estimated 370 000 [230 000–510 000] children were newly infected with HIV in 2009 (a drop of 24% from five
