Catholic Medical Quarterly

The Journal of the Catholic Medical Association (UK)

Building knowledge. Building faith. Protecting the vulnerable.

Catholic Medical Quarterly Volume 63(3) August 2013

HIV Transmission and Condoms

Dr John Mclean, Manchester


In July 2012 twenty five thousand delegates attended the 19th International AIDS Conference in Washington, DC (1). As reported during the conference there are approximately 34 million people currently living with HIV and nearly 30 million people have died of AIDS related causes since the beginning of the epidemic. While cases have been reported in all regions of the world, 97% of those living with the infection reside in low and middle income countries and over two thirds of those infected (69%) live in sub-Saharan Africa which accounts for only 12% of the world’s population. Globally half of all HIV infections occur in women and in sub-Saharan Africa women account for 60% of those infected (2). These figures may not reflect the true severity of the epidemic since the Joint United Nations Programme on HIV/AIDS (UNAIDS) and other prominent sources of data report prevalence rates only for those aged 15–49 years, and the indicators used by the United Nations General Assembly Special Session focus predominantly on the same age group (3). Furthermore, the necessary diagnostic tests for HIV infection are not readily available in some African countries.

Background information

An apparently new disease affecting the immune system was the subject of two reports published in the New England Journal of Medicine in 1981. One report concerned several young men who had died as the result of an unusual form of pneumonia caused by the organism Pneumocystis carinii. The other reported the deaths of young men as a result of the relatively rare tumour, Kaposi Sarcoma. The only common factor was that those who died had been involved in homosexual activity.

In 1981 the US Centers for Disease Control (CDC) reported an increased incidence of Kaposi Sarcoma (KS), Pneumocystis carinii pneumonia (PCP) and overwhelming yeast infections in homosexual men, intravenous drug users and the recipients of blood transfusions or blood products. It was assumed that a deficiency in the immune system, whatever the cause, rendered these individuals vulnerable to such infections and the CDC named the condition Acquired Immune Deficiency Syndrome, hence the acronym AIDS.

In 1983 Luc Montagnier and colleagues at the Pasteur Institute in France isolated a retrovirus from the lymph nodes of a homosexual male dying with AIDS and named it LAV (lymphadenopathy-associated virus). In 1984 Robert Gallo and colleagues at the National Institute of Health in the USA isolated a comparable retrovirus from a similar patient and called it HTLV (human T cell lymphotrophic virus). In 1986 it was decided that this virus be called the human immunodeficiency virus or HIV.

Initially the diagnosis of HIV/AIDS was dependent on the presence of overwhelming infection, usually PCP or Thrush. In 1985 a simple test for the viral antibody became available and more sophisticated tests and investigations were subsequently developed. After their introduction the level of infection was monitored by the number of viral particles in the circulation, (viral load per unit volume), and following the development of effective antiretroviral drugs, the response to treatment was monitored by falling viral loads and rising CD4 cell counts, the CD4 T lymphocytes (helper cells) being essential to an effective immune response to viral infection.

All viruses have target cells: influenza viruses target the lining epithelial cells of the respiratory tract; hepatitis viruses target liver cells while herpes simplex viruses and human papilloma viruses target skin cells. Unfortunately HIV, which is a retrovirus, targets the CD4 cells of the immune system. It is termed a retrovirus because it possesses an enzyme ‘reverse transcriptase’ which, when the virus enters the target CD4 cell, allows it to convert its genetic RNA into DNA. The viral RNA, now converted into DNA, enters the CD4 cell’s nucleus and is incorporated into the CD4 cell’s nuclear DNA. The normal metabolic activity of the infected CD4 cell allows the viral DNA to replicate itself which then reverts to its original viral RNA form. These RNA transcripts leave the CD4 cell nucleus and another viral enzyme, protease, reassembles the viral particles in the CD4 cell’s cytoplasm. This process causes the death of the CD4 cell and releases large numbers of viral particles into the blood.

Initially the CD4 cells are replenished as quickly as they are destroyed but eventually the CD4 cell count, normally 1000 cells per unit volume of blood, begins to fall and the infected individual becomes vulnerable to overwhelming opportunistic infection and tumour formation. Before the development of effective antiretroviral drugs the treatment of patients with HIV infection was limited to the treatment of the opportunistic infections. The subsequent development of effective drug therapy has converted HIV infection into a chronic disease which requires continuous medication and monitoring. Several different groups of antiretroviral drugs are available for treatment and initial medication involves three drugs, two from one group and a third from a different group (4). Monitoring of the patient’s response to treatment is essential because constant viral mutation may render one or other of the drugs ineffective. Indeed the increased availability of antiretroviral treatment for HIV infected patients in sub-Saharan Africa has been accompanied by rising rates of drug resistance which is a potential threat to the worldwide control of HIV/AIDS. This situation has arisen because of the widespread use of low cost substandard drug regimens, restricted access to monitoring of viral load, treatment interruptions when drugs are not available and suboptimal long term adherence (5).

Transmission of infection

The virus is present in the body fluids, lymphoid cells and other cells of an infected individual. The three principal modes of transmission are:

  • Blood, blood products and contaminated instruments which put at risk IV drug users and those exposed to injections, tattooing needles, acupuncture and scarification.
  • Sexual, any form of sexual activity which involves vaginal, oral and anal penetration, including oral- genital and oral-anal contact.
  • Mother to child: in utero, during labour and breastfeeding.

In the developing world transmission of HIV infection occurs mainly during normal heterosexual intercourse. The reasons for this are fourfold:

  • Malnutrition, apart from its debilitating effect on general health, is specifically responsible for impairing the barrier function of the skin and renders the lining epithelium of the vagina less effective as a barrier to infection.
  • The common sexually transmitted diseases occur worldwide and without adequate treatment lead to chronic ill health. If these STDs are ulcerating in character, as they are in equatorial regions, the barrier to infection is non-existent.
  • Endemic parasitic disease is common in many developing countries and imposes a significant burden on an immune system perhaps further impaired by malnutrition.
  • Inadequate maternal care results in damage to the female reproductive tract during labour and reduces its effectiveness as a barrier to infection during subsequent sexual intercourse.

Policies to reduce transmission

Numerous agencies (UNAIDS, WHO, etc) promote education and condom use as the most effective means of controlling the HIV epidemic in developing countries. Educational programmes may be categorised as either ‘risk reduction’ or ‘risk avoidance’. Risk reduction models promote condom use and effective treatment of sexually transmitted infections thereby avoiding the imposition of ethical or moral codes and value judgements. Risk avoidance models promote premarital abstinence, monogamy, fidelity and concern behavioural change.

Condom Use

The contraceptive failure rate of condoms is 10-15% over one year (6). Consistent use of condoms between heterosexual partners one of whom is HIV positive reduces the risk of transmission by 85% (7) or 80% (8). The authors of this second paper conclude that condom effectiveness with regard to HIV transmission is similar to, although lower than that for contraception. The conclusion from studies of stable couples in the developed world is that male-to-female transmission is approximately twice as efficient as female-to-male transmission (9)

The effectiveness of condoms was questioned in a Lancet leading article in 1994 (10) referencing a study which suggested that consistent use of condoms may reduce the risk of transmission between infected and non-infected heterosexual partners by an estimated 69% (11). In 2003 the public health benefit of condom promotion in settings with widespread heterosexual transmission of HIV remained unclear because reducing the number of partners appeared to be more important than condoms in curbing the epidemic in Uganda (12). In the same year Dr E C Green of Harvard’s Centre for Population and Development Studies stated that ‘Twenty years into the epidemic there is no evidence that more condoms leads to less AIDS (13). Also in 2003 Hearst and Chen of the University of California conducted a condom effectiveness study for the United Nation’s AIDS programme and found no evidence of condoms working as a primary HIV-prevention measure in Africa (14). UNAIDS quietly disowned the study (15). Since then, major articles in other peer-reviewed journals such as the Lancet, Science and the BMJ have confirmed that condoms have not worked as a primary intervention in the population-wide epidemics in Africa (15). The authors of the Science article concluded that ‘consistent condom use has not reached a sufficiently high level, even after many years of widespread and often aggressive promotion, to produce a measurable slowing of new infections in the generalised epidemics of sub-Saharan Africa’ (16).

Condom Failure

As a contraceptive, condoms fail to prevent pregnancy in 10-15 of 100 women during the first year of use (6). Following contraceptive failure many women have recourse to abortion. Thus of 182 women who had been using condoms for contraception 100 pregnancies were aborted due to method failure and 82 because of poor compliance (17). When condoms are used to prevent the transmission of HIV, a method failure or one due to poor compliance may not be recognised nor declare itself two weeks later.

When condoms fail to prevent conception and the transmission of HIV they do so because of:

  • Innate deficiencies in the latex material used in their manufacture (method failure)
  • Failure to use them during every act of sexual intercourse (poor compliance)
  • Rupture during sexual intercourse (method failure)
  • Inexperience in their use (poor compliance and method failure)
  • Cultural resistance to their use (poor compliance)

A major problem consequent on the promotion of condoms as a means of preventing HIV transmission is the assumption that they are 100% effective since this affords the user a false sense of security. It has been further suggested that the availability of condoms generates behaviour change, increasing both the frequency of sexual intercourse and the number of partners (18).

When condoms fail to prevent conception it is often due to method failure (17). A WHO/UNAIDS source claims the failure rate for perfect condom use is approximately 3% and for typical use is 12% (19) Although rupture of a condom during sexual intercourse is evident to the user, leakage of ejaculate through an apparently intact condom is unlikely to be recognised. Although the use of condoms to prevent conception and HIV transmission are comparable there are important differences. Conception can only occur as a result of vaginal intercourse during a few days of the woman’s menstrual cycle while HIV can be transmitted by vaginal, oral and anal routes and can occur at any time. Furthermore the human immunodeficiency virus is smaller than spermatozoa and may leak through apparently intact condoms. In vitro trials have demonstrated HIV leakage in 0-100% of the condoms tested (11, 20, 21, 22, 23, 24).

Another important aspect of the HIV epidemic in Africa concerns its effect on children. In 2011 there were 3.4 million children living with HIV of whom 91% were in sub-Saharan Africa. In 2009 there were approximately 16.6 million AIDS orphans, children who have lost one or both parents to HIV infection, 89% of whom were in sub-Saharan Africa (2).


  1. Kamerow D, The myth of an AIDS free world. British Medical Journal, (18 August) 2012; 345 31. Cite this as: BMJ 2012;345:e5479
  2. U.S. Global Health Policy Fact Sheet July 2012.
  3. Negin J, Cumming R G, HIV infection in older adults in sub-Saharan Africa: extrapolating prevalence from existing data. Bulletin of the World Health Organisation 2010; 88: 847-853.
  4. British HIV Association Guidelines for the treatment of HIV-1 positive adults with antiretroviral therapy, 2012.
  5. Hamers R L et al. Global threat from drug resistant HIV in sub-Saharan Africa. British Medical Journal, (21 July) 2012; 345: 29-31. Cite this as: BMJ 2012;344:e4159
  6. Contraceptive Use: Facts in Brief. Alan Guttmacher Institute, March 2005.
  7. US National Institute of Health Report, 2000.
  8. Weller S C, Davis-Beaty K, The Cochrane Library 2007, Issue 4.
  9. Haverkos H W, Battjes R J, Female-to male transmission of HIV. Journal of the American Medical Association 1992; 268: 1855.
  10. Johnson M D, Condoms and HIV transmission. Lancet, 1994; 331 (6) 391-392.
  11. Weller S C, A meta-analysis of condom effectiveness in reducing sexually transmitted HIV. Social Science and Medicine, 1993; 36: 1635-44.
  12. UNAIDS Review 2003
  13. UNAIDS Review 2003
  14. Hearst N, Chen S, Condom Promotion for AIDS Prevention in the Developing World: Is It Working? Studies in Family Planning, 2004; 35 (1): 39-47.
  15. Green E C, The Pope may be right. The Washington Post Sunday March 29, 2009.
  16. Potts M et al. Reassessing HIV Prevention. Science, 2008; 320 (5877): 749-750.
  17. Griffiths M, Contraceptive practices and contraceptive failures among women requesting termination of pregnancy. The British Journal of Family Planning, 1990; 16: 16-18.
  18. Richens J, Imrie J, Copas A, Condoms and seat belts: the parallels and the lessons. Lancet, 2000; 355: 400-403.
  19. WHO/UNAIDS The male latex condom Fact Sheets, No 1.
  20. Voeller B, Nelson J, Day C, Viral leakage risk differences in latex condoms. AIDS Research and Human retroviruses, 1994; 10 (6): 701-710.
  21. Carey R F et al. Effectiveness of latex condoms as a barrier to human immunodeficiency virus-sized particles under conditions of simulated use. Sexually Transmitted Diseases, 1992; 19 (4): 230-234.
  22. Judson F L et al. In vitro evaluations of condoms with and without nonoxynol 9 as physical and chemical barriers against Chlamydia trachomatis, herpes simplex virus type 2 and human immunodeficiency virus. Sexually Transmitted Diseases, 1989; 16 (2): 51-56.
  23. Reitmeijer C A M et al. Condoms as physical and chemical barriers against human immunodeficiency virus. Journal of the American Medical Association, 1988; 259 (12): 1851-1853.
  24. Lytle C D et al. Virus leakage through natural membrane condoms. Sexually Transmitted Diseases, 1990; 17(2) 58-62.