**3. Vertical or Mother To Child Tranmission (MTCT)**

The major source of paediatric infection of Human immunodeficiency virus one (HIV-1) is from mother to child. Since the first reported case of HIV-1 transmission in children in 1983, the global pandemic has had a serious impact on the health and survival of children. Transmission rates have been reported to be about 14% in industrialised countries and about 35-45% in developing countries especially in Africa (Bryson, 1996; Reinhardt et al., 1995).

It was estimated that MTCT accounts for over 1.5million HIV infection in children (Burton, 1996) with the WHO projecting between 5-10million child infections through MTCT during the next decade. HIV-2 though is related to HIV-1 is less readily transmitted from mother to child, this could be attributed to their differences which influences pathogenecity, natural history and therapy so that their susceptibility to antiretroviral therapy (ART) follows different mutation pathways to develop drug resistance (Mamata and Merchant, 2010).

According to Wollinsky et al (1992) as quoted by Pasquier et al (1998), the transmission of HIV-1 from mother to child occur *utero*, *intrapartum*, or postnatally by breastfeeding and a fourth dimension as reported by Pasquier et al (1998) which involves the transmission of multiple maternal variants to the infant and a rapid, fatal outcome in the child and the development of an HIV-based clinical disease in children seems to be correlated with the timing of the vertical transmission.

Infection in about two-thirds of children are thought to have occurred at the terminal end of pregnancy or at delivery with the disease progressing slowly; while in one-thirds, it is thought to progress rapidly to AIDS with increased indices of viral replication (De Rossi et al., 1998), these children appear to have been infected during pregnancy.

Infected children with slow progression to AIDS have a higher viral diversity than children who progress rapidly as evidenced in molecular variability studies (Halapi et al., 1996; Strunnikora et al., 1995) as reported in Adults (Delwart et al., 1997; Pasquier et al., 1998).

Although progress has been made in recent years in the curbing of MTCT, the mechanisms and timing of transmission remains uncertain and the relative contributions of each of the three modes of transmission is still not well defined. Bryson et al (1992) proposed that in most non-breastfeeding population; the lack of detection of virus in the child at birth might indicate that contamination took place at or shortly before delivery while detection of virus at birth indicates *utero* contamination. Evidences for both early and late utero transmission have been documented (Peckham and Gibb, 1995; Kuhn and Stein, 1995). Most prior estimates and hypothesis seem to agree that transmission usually occur during the *intrapartum* HIV exposure just as premature infants.

Perinatal or *Antepartum* HIV transmission has been documented as a route of infection estimated to occur in 13-30% of infants delivered to HIV-1 infected mothers (Andiman et al., 1990).

High proviral DNA/ or RNA concentration of virus is a risk factor for the transmission of HIV-1 from an untreated mother to infant. The reduction in such transmission after zidovudine is only partly explained by the reduction in plasma levels of viral RNA. To prevent HIV-1 transmission initiating maternal treatment with zidovudine is recommended regardless of the plasma level of HIV-1 RNA or the CD4+ Count (Sperling et al., 1996). Because of the different mutation pathways to develop drug resistance, pregnant women with detectable HIV-2 should be ideally managed using a Highly Active antiretroviral therapy (HAART) regimen to which the virus is sensitive. Non-nucleoside Reverse

The major source of paediatric infection of Human immunodeficiency virus one (HIV-1) is from mother to child. Since the first reported case of HIV-1 transmission in children in 1983, the global pandemic has had a serious impact on the health and survival of children. Transmission rates have been reported to be about 14% in industrialised countries and about 35-45% in developing countries especially in Africa (Bryson, 1996; Reinhardt et al.,

It was estimated that MTCT accounts for over 1.5million HIV infection in children (Burton, 1996) with the WHO projecting between 5-10million child infections through MTCT during the next decade. HIV-2 though is related to HIV-1 is less readily transmitted from mother to child, this could be attributed to their differences which influences pathogenecity, natural history and therapy so that their susceptibility to antiretroviral therapy (ART) follows different mutation pathways to develop drug resistance (Mamata and Merchant, 2010). According to Wollinsky et al (1992) as quoted by Pasquier et al (1998), the transmission of HIV-1 from mother to child occur *utero*, *intrapartum*, or postnatally by breastfeeding and a fourth dimension as reported by Pasquier et al (1998) which involves the transmission of multiple maternal variants to the infant and a rapid, fatal outcome in the child and the development of an HIV-based clinical disease in children seems to be correlated with the

Infection in about two-thirds of children are thought to have occurred at the terminal end of pregnancy or at delivery with the disease progressing slowly; while in one-thirds, it is thought to progress rapidly to AIDS with increased indices of viral replication (De Rossi et

Infected children with slow progression to AIDS have a higher viral diversity than children who progress rapidly as evidenced in molecular variability studies (Halapi et al., 1996; Strunnikora et al., 1995) as reported in Adults (Delwart et al., 1997; Pasquier et al., 1998). Although progress has been made in recent years in the curbing of MTCT, the mechanisms and timing of transmission remains uncertain and the relative contributions of each of the three modes of transmission is still not well defined. Bryson et al (1992) proposed that in most non-breastfeeding population; the lack of detection of virus in the child at birth might indicate that contamination took place at or shortly before delivery while detection of virus at birth indicates *utero* contamination. Evidences for both early and late utero transmission have been documented (Peckham and Gibb, 1995; Kuhn and Stein, 1995). Most prior estimates and hypothesis seem to agree that transmission usually occur during the

Perinatal or *Antepartum* HIV transmission has been documented as a route of infection estimated to occur in 13-30% of infants delivered to HIV-1 infected mothers (Andiman et al.,

High proviral DNA/ or RNA concentration of virus is a risk factor for the transmission of HIV-1 from an untreated mother to infant. The reduction in such transmission after zidovudine is only partly explained by the reduction in plasma levels of viral RNA. To prevent HIV-1 transmission initiating maternal treatment with zidovudine is recommended regardless of the plasma level of HIV-1 RNA or the CD4+ Count (Sperling et al., 1996). Because of the different mutation pathways to develop drug resistance, pregnant women with detectable HIV-2 should be ideally managed using a Highly Active antiretroviral therapy (HAART) regimen to which the virus is sensitive. Non-nucleoside Reverse

al., 1998), these children appear to have been infected during pregnancy.

*intrapartum* HIV exposure just as premature infants.

**3. Vertical or Mother To Child Tranmission (MTCT)** 

1995).

1990).

timing of the vertical transmission.

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).

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 of vertical transmission (Al-husaini, 2009).

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 years earlier)[UNAIDS, 2010].

Human Immunodeficiency Virus Transmission 49

as well which are thought to occur when the infant ingests the mothers blood through a

Other known correlates include high maternal plasma viremia, advanced clinical HIV disease, degraded maternal immunocompetence or prolonged rupture of the amniotic membranes before delivery. Others include vaginal delivery process and prematurity of low

High frequency of sexual activity and ''hard'' drug injection during pregnancy had previously been identified, along with unprotected sexual intercourse during pregnancy as certain behavioural risk factors for mother-to-child-transmission (Bulterys et al., 1997; Bulterys and Goedert, 1996). Firstly, unprotected intercourse might increase the concentration of strain diversity of HIV-1, particularly in the birth canal where ejaculated virus could be partially sequestered. Secondly, frequent intercourse might increase inflammation of the cervix or vagina either micro abrasion or if unprotected, by STDs. Third, frequent intercourse might increase the risk of chorioamnionitis or otherwise alter the integrity of the placenta (Bulterys and Goedert, 1996). Matheson et al (1997) found that continued drug users had significantly higher mother-to-child-transmission rates in maternal drug use during pregnancy. However, this was confounded by other variables such as premature delivery, prolonged membrane rupture, zidovudine non-use and

In the USA, cigarettes' smoking during pregnancy has been identified as independent risk factor for mother-to-child-transmission. The effect was greatest among women with critical evidence of more advanced HIV disease (Turner et al., 1996). Intensive nurse care management in supporting zidovudine use in women with HIV infection and their infants is a proven effective method in decreasing mother-to-child-transmission (Havens et al., 1997). MTCT of HIV is influenced by multiple factors. Known correlates include high maternal plasma viremia, advanced clinical HIV disease, degraded maternal immunocompetence or prolonged rupture of the amniotic membranes before delivery. Others include vaginal delivery process and prematurity of low birth weight of the neonate (Bryson 1996; John and

Results from zidovudine therapy to bridge MTCT have improved understanding of the pathophysiology of MTCT. First, the reduction in plasma viremia and MTCT (from 25.5% to 8.3%) by treating the mother and neonates suggests that relatively small changes in maternal viral load might have substantial effects on MTCT (Bulterys and Godert 1996; CDC, 1994). Secondly, cleaning of birth canal with chlorhexidine had no overall effect yet apparently did reduce MTCT for one subgroups of high-risk deliveries; those after 4hrs of membrane

Maternal immunologic and virologic factors such as quantitative HIV-1 RNA (though insufficient) are strongly correlated with Mother-to-child-transmission. When stratified by the stage of HIV disease, the only group with significant association between viral load and mother-to-child-transmission were AIDS-free women with high CD4+ Counts. The interactions of virus burden and maternal immune status has also demonstrated that CD4+, CD8+ cell subsets are percentages of CD8+ cell subsets (e.g. activation markers CD8/CD38 and CD8/DR) were all associated with vertical transmission. Women in the highest CD4+ cell percentage quartile or the lowest CD8+ cell percentage quartile had only less than or

equal to 4 percent of mother-to-child-transmission (Njoku, 2004).

birth weight of the neonate (Bryson, 1996; John and Kreiss, 1996; Lambert, 1996).

cracked and bleeding nipples.

unprotected sexual intercourse.

Kreiss, 1996; Lambert, 1996).

rupture (Scarlatti, 1996).

#### **4. Risk factors for vertical transmission of HIV**

Documented evidence primarily based on PCR and virus culture studies or co-culture studies but short of serology which revealed maternal antibodies present in infants at birth showed that transmission of HIV from mother to child appears to occur in 11-60% of children delivered by HIV-positive mothers but reasons for the wide variations in virus transmission and sources of virus in newborn which could have provided approach to prevention are not known (Ades et. al., 1991; Courgnaud et. al., 1991; Lindgren et. al., 1991; Newell et. al., 1992; Scarlatti et. al., 1991; Tovo and Martino, 1988; Oxtoby, 1990; Rogers et. al., 1991).

Maternal, viral, obstetric, foetal, infant factors all affect transmission making it essentially multifactorial. Frequency of sexual activity, 'hard' drug ingestion during pregnancy, unprotected sexual intercourse, cigarette smoking during pregnancy, lack of adherence to drugs, HIV disease, degraded maternal immunocompetence or prolonged rupture of the amniotic membranes before delivery (Havens et al., 1997; Turner et al., 1996; Bryson, 1996; John and Kreiss, 1996; Lambert, 1996; Glenn and Dietrich, 1993).

The maternal factors involve transmission through the placenta to the unborn child, at the time of labour and delivery, or through breast-feeding. (CDC HIV/AIDS surveillance, October, 1989), seroconversion during pregnancy, advanced stage of the disease with high viral load and low immunity, concomitant malnutrition, micronutrient deficiencies, sexually transmitted diseases, no or suboptimal therapy; in the intranatal period, risk factors for increased transmission are mode of delivery, prolonged contact with maternal blood or cervicovaginal secretions, prolonged rupture of membranes, chorioamnionitis, invasive procedures like episiotomy, foetal scalp electrode, instrumental delivery; thin skin, susceptible mucous membranes, immature immune functions and low levels of maternal antibodies make prematurity a risk factor for increased transmission. In the postnatal period, risk factors are breast feeding, feeding with cracked nipples/mastitis, mixed feeding, new seroconversion of the mother, high viral load, low CD4 cell count; In the absence of any intervention, rates of MTCT of HIV-1 can vary from 15 to 30% in developed countries and increase to 30 to 45% in developing countries, the difference mainly attributable to infant feeding practices that comprise almost universally of breastfeeds for prolonged duration (De Cock et al., 2000 as quoted by Mamata and Merchant, 2001).

The foetus and mother circulatory systems though different, there still exists tiny mixing of blood that could serve as portal for the flow of infected maternal white blood cells or the AIDS virus in the maternal serum to be transmitted to the foetus with a confirmation found in the foetal tissues affirming such spread (CDC HIV/AIDS surveillance, October 1989; Glenn and Dietrich, 1993).

Bruising, abrasions and local swelling could occur to the baby and mother during labour owing to a great deal of trauma which produces visible and microscopic openings that could allow the virus to penetrate blood stream of infant. Another means of infection could be experienced or seen when the mother's perineum tears or if she receives an episiotomy which might lead to a large amounts of blood ingested by the baby or might get into the baby's mouth, eyes, rectum or vagina.

Glenn et al (1993) reported that breastfeeding is another means of risks exposure and it has been confirmed in the spread of hepatitis B from mother to infant and hepatitis B and AIDS

Documented evidence primarily based on PCR and virus culture studies or co-culture studies but short of serology which revealed maternal antibodies present in infants at birth showed that transmission of HIV from mother to child appears to occur in 11-60% of children delivered by HIV-positive mothers but reasons for the wide variations in virus transmission and sources of virus in newborn which could have provided approach to prevention are not known (Ades et. al., 1991; Courgnaud et. al., 1991; Lindgren et. al., 1991; Newell et. al., 1992; Scarlatti et. al., 1991; Tovo and Martino, 1988; Oxtoby, 1990; Rogers et.

Maternal, viral, obstetric, foetal, infant factors all affect transmission making it essentially multifactorial. Frequency of sexual activity, 'hard' drug ingestion during pregnancy, unprotected sexual intercourse, cigarette smoking during pregnancy, lack of adherence to drugs, HIV disease, degraded maternal immunocompetence or prolonged rupture of the amniotic membranes before delivery (Havens et al., 1997; Turner et al., 1996; Bryson, 1996;

The maternal factors involve transmission through the placenta to the unborn child, at the time of labour and delivery, or through breast-feeding. (CDC HIV/AIDS surveillance, October, 1989), seroconversion during pregnancy, advanced stage of the disease with high viral load and low immunity, concomitant malnutrition, micronutrient deficiencies, sexually transmitted diseases, no or suboptimal therapy; in the intranatal period, risk factors for increased transmission are mode of delivery, prolonged contact with maternal blood or cervicovaginal secretions, prolonged rupture of membranes, chorioamnionitis, invasive procedures like episiotomy, foetal scalp electrode, instrumental delivery; thin skin, susceptible mucous membranes, immature immune functions and low levels of maternal antibodies make prematurity a risk factor for increased transmission. In the postnatal period, risk factors are breast feeding, feeding with cracked nipples/mastitis, mixed feeding, new seroconversion of the mother, high viral load, low CD4 cell count; In the absence of any intervention, rates of MTCT of HIV-1 can vary from 15 to 30% in developed countries and increase to 30 to 45% in developing countries, the difference mainly attributable to infant feeding practices that comprise almost universally of breastfeeds for prolonged duration (De Cock et al., 2000 as quoted by Mamata and

The foetus and mother circulatory systems though different, there still exists tiny mixing of blood that could serve as portal for the flow of infected maternal white blood cells or the AIDS virus in the maternal serum to be transmitted to the foetus with a confirmation found in the foetal tissues affirming such spread (CDC HIV/AIDS surveillance, October 1989;

Bruising, abrasions and local swelling could occur to the baby and mother during labour owing to a great deal of trauma which produces visible and microscopic openings that could allow the virus to penetrate blood stream of infant. Another means of infection could be experienced or seen when the mother's perineum tears or if she receives an episiotomy which might lead to a large amounts of blood ingested by the baby or might get into the

Glenn et al (1993) reported that breastfeeding is another means of risks exposure and it has been confirmed in the spread of hepatitis B from mother to infant and hepatitis B and AIDS

**4. Risk factors for vertical transmission of HIV** 

John and Kreiss, 1996; Lambert, 1996; Glenn and Dietrich, 1993).

al., 1991).

Merchant, 2001).

Glenn and Dietrich, 1993).

baby's mouth, eyes, rectum or vagina.

as well which are thought to occur when the infant ingests the mothers blood through a cracked and bleeding nipples.

Other known correlates include high maternal plasma viremia, advanced clinical HIV disease, degraded maternal immunocompetence or prolonged rupture of the amniotic membranes before delivery. Others include vaginal delivery process and prematurity of low birth weight of the neonate (Bryson, 1996; John and Kreiss, 1996; Lambert, 1996).

High frequency of sexual activity and ''hard'' drug injection during pregnancy had previously been identified, along with unprotected sexual intercourse during pregnancy as certain behavioural risk factors for mother-to-child-transmission (Bulterys et al., 1997; Bulterys and Goedert, 1996). Firstly, unprotected intercourse might increase the concentration of strain diversity of HIV-1, particularly in the birth canal where ejaculated virus could be partially sequestered. Secondly, frequent intercourse might increase inflammation of the cervix or vagina either micro abrasion or if unprotected, by STDs. Third, frequent intercourse might increase the risk of chorioamnionitis or otherwise alter the integrity of the placenta (Bulterys and Goedert, 1996). Matheson et al (1997) found that continued drug users had significantly higher mother-to-child-transmission rates in maternal drug use during pregnancy. However, this was confounded by other variables such as premature delivery, prolonged membrane rupture, zidovudine non-use and unprotected sexual intercourse.

In the USA, cigarettes' smoking during pregnancy has been identified as independent risk factor for mother-to-child-transmission. The effect was greatest among women with critical evidence of more advanced HIV disease (Turner et al., 1996). Intensive nurse care management in supporting zidovudine use in women with HIV infection and their infants is a proven effective method in decreasing mother-to-child-transmission (Havens et al., 1997).

MTCT of HIV is influenced by multiple factors. Known correlates include high maternal plasma viremia, advanced clinical HIV disease, degraded maternal immunocompetence or prolonged rupture of the amniotic membranes before delivery. Others include vaginal delivery process and prematurity of low birth weight of the neonate (Bryson 1996; John and Kreiss, 1996; Lambert, 1996).

Results from zidovudine therapy to bridge MTCT have improved understanding of the pathophysiology of MTCT. First, the reduction in plasma viremia and MTCT (from 25.5% to 8.3%) by treating the mother and neonates suggests that relatively small changes in maternal viral load might have substantial effects on MTCT (Bulterys and Godert 1996; CDC, 1994). Secondly, cleaning of birth canal with chlorhexidine had no overall effect yet apparently did reduce MTCT for one subgroups of high-risk deliveries; those after 4hrs of membrane rupture (Scarlatti, 1996).

Maternal immunologic and virologic factors such as quantitative HIV-1 RNA (though insufficient) are strongly correlated with Mother-to-child-transmission. When stratified by the stage of HIV disease, the only group with significant association between viral load and mother-to-child-transmission were AIDS-free women with high CD4+ Counts. The interactions of virus burden and maternal immune status has also demonstrated that CD4+, CD8+ cell subsets are percentages of CD8+ cell subsets (e.g. activation markers CD8/CD38 and CD8/DR) were all associated with vertical transmission. Women in the highest CD4+ cell percentage quartile or the lowest CD8+ cell percentage quartile had only less than or equal to 4 percent of mother-to-child-transmission (Njoku, 2004).

Human Immunodeficiency Virus Transmission 51

semen viral load (Gupta et al., 1997; Tachet et al., 1999; Kalichman et al., 2008; Butler et al., 2008), stage of HIV infection (Mastro et al., 1994; Fauci et al., 1996; Wawer et al., 2005), comorbid sexually transmitted diseases (Royce et al., 1997), vaginal or anal canal, co-occurring

Sexual forms of transmission are seen as a major portal of entry of HIV as 10-30% of seminal/vaginal fluids have transmissible virus (Royce et al., 1997; Henin et al., 1993). In semen viral load, the males HIV-1 infected cells forms about 104 of the 106 leucocytes per ejaculation (Winkelstein et al., 1987), which confirms AIDS first association with sexual route, with the high prevalence in homosexual men. The virus subsequently became synonymous with heterosexual activity and is now attributed to the AIDS pandemic (UNAIDS 1986; Nkowane 1991; Stoneburner et al., 1990). Bouvier et al (1997) believes that

The chances of transmission also depends on the type of sexually transmitted infections (STI), as co-infection with genital ulcers have been reported to increase the chances of transmission by increasing the susceptibility to HIV infection which also depends on HIV subtypes efficient (Gray et al., 2001; Mahiane et al., 2009; Limpakarnianarat et al., 1993;

Male circumcision have been documented to decrease the chances of HIV transmission (Mahiane et al., 2009; Lavreys et al., 1999; Gray et al., 2000; Reynolds et al., 2004; Gray et al., 2007; Donoval et al., 2006), but this also depends on the country (Ben et al., 2008; Sullivan et

The high level of heterosexual spread of HIV in Sub-Saharan Africa and developing countries where genital ulcers from existing venereal diseases (e.g. Chanchroid Chlamydia, Syphilis or Herpes virus infections) are aligned with increased HIV seroprevalence (UNAIDS, 1998, Hook et al., 1992; Plummer et al., 1991) could be tight to abrasions at the site of entry in the vagina or anal canal. Heise et al (1991) however reported that HIV could directly infect the bowel mucosa and perhaps cervical epithelium without the need for ulcerations which gave clue to the relatively low risk of the mucosal lining of the foreskin, urethral canal and oral genital contact (through minimal) to be implicated (Winkelstein et

Men having Sex with Men (MSM) have been reported as one of the first way of transmission of HIV. Various authors have showed evidence that the involvement of MSM could be traced to psychosocial behaviour (PB). These PB are said to be depression, violent victimisation, substance abuse, alcohol, psychiatric disorders, psychological distress, lower perceived social support (Berlan et al., 2010; King et al., 2008; Meyer , 2003; Cochran et al., 2003; Cochran and Mays, 2000; Gilman et al., 2001., Marshal et al., 2008; Mimiaga et al., 2009a; b; Safren and Heimberg, 1999; Stall et al., 2001; Chesney et al., 2003; The EXPLORE Study Team, 2004; Herbst et al., 2005). Although some studies have shown how substance use and high risk of HIV transmission are correlated (Stall et al., 2001; Hirshfield et al., 2004), most recent studies are now focussing on how *'syndemic'*- a situation where these diverse psychosocial issues could interact to enhance HIV risky behaviour among MSM (Mustanski et al., 2007; 2010; Stall et al., 2008; Centers for Disease Control and Prevention, 2010). However, varieties of cognitive behavioural interventions have been studied and validated for the treatment of mood and anxiety disorders (Barlow, 2008) behavioural activation therapy and HIV risk reduction counselling in MSM who abuse crystal

vaginal pH neutralization by semen is a co-factor of HIV transmission.

psychosocial risk factors (Safren et al., 2010).

al., 2009; Ruan et al., 2009; Wawer et al., 2009).

methamphetamine (Mimiaga et al., 2010).

Wang, 2009; Xu, 2009).

al., 1987).
