What’s in Your Genes?

Student guest post by Liz Stepniak

In the field of chronic disease, genetics has long been determined as a component of disease susceptibility. Infectious disease was believed to be caused by an agent of infection, such as a virus or bacteria which comprises a large environmental factor. In the past decade or so, this view has been expanded to include an important genetic factor as well.

There has been scientific evidence supporting the controversial idea that one error in a single gene can significantly alter the individual’s risk of obtaining a bacterial infection. Can infectious disease develop as a result of such genetic vulnerabilities? This idea was met with resistance from the microbiology field, which stresses that infectious diseases are strictly environmental. Immunologists have also viewed this idea with skepticism; since adding this component opens a large area of re-exploration for the possibilities of interactions between a range of microbes and certain immunological molecules. The positive implications of further research in this area is that it allows for a more complete and accurate way of treating infection. This also opens the door to further explanation of the immune system as a target for treatment instead of just the bacteria causing the infection.

There are many important components of infectious disease, but I’m going to focus on disease severity for the research I’m going to discuss further. This is by no means an exhaustive commentary, merely a discussion of a few papers I found interesting while I was looking into this topic and what it could bring to the scientific and medical worlds:
A study published in December 2008 took the first look into genetic determinants of severity of acute infectious illnesses. These researchers found that high-risk gene combinations made certain individuals 8 times more likely to suffer from a severe and prolonged illness. Another interesting result from this paper was that the converse was also true, a certain gene combination acted protectively; with these individuals having a less severe, shorter illness. I thought this was an interesting paper because in the future, it may be possible to identify those individuals at high-risk and provide prevention and more appropriate treatment for common infectious disease.

Recent research findings from Rockefeller University and the Necker Medical School that supports this idea has identified a new gene mutation that causes children to be more susceptible to mycobacterial diseases. Mycobacterium infection can lead to diseases like leprosy or tuberculosis. This January 2010 paper suggested that this mutation disrupts IFN- γR1, which is responsible for making a receptor for interferon γ, a molecule that leads the immune cells to form an attack on a foreign organism. It has been found that when this receptor is absent or not fully functional, an immune system pathway that specifically targets mycobacterium is disrupted. This was a small study, only done in 118 patients with complete or partial IFN-γR1 deficiency; but 33 different IFN-γR1 mutations were found among these patients.

A researcher conducting this study explained that the severity of the disease depended on the severity of the deficiency, and that for this deficiency; there was little difference between partial and complete deficiency leading to a dramatic increase in the severity of the mycobacterial disease. For one young patient, the researchers sequenced the genes of this patient and her healthy family members. They found that each parent had one copy of the mutation located on the initiation codon. This article also provided further evidence to the idea that an error in a single gene may be enough to radically alter individual risk for bacterial disease. This research group, led by Jean Laurent Casanova has also conducted research studies showing underlying genetic vulnerabilities to other infectious diseases including pneumococcal disease and herpes simplex encephalitis.

I found this topic interesting because a lot of important efforts focus on altering environmental factors that cause disease but the strong presence of a genetic component just keeps sneaking into all forms of disease and illness and adding a complexity to understanding and treatment. It just goes to show how interactive the battle between the human body and infectious agents has become! While there have been multiple studies demonstrating the important role of genetics in infectious disease, there is further evidence needed to better understand the multifaceted puzzle that results from the interactions of genetics, environments, and infectious agents with regards to all disease components. As with most research, the more discoveries investigators make, the more it makes us realize is still out there to be uncovered and understood. Even though this may add to the difficulty of understanding infectious diseases; with more research in this area, the outcome can lead to better treatments and prevention efforts of infectious diseases and more lives saved.

Works Cited:

Kong et al. (2010). A novel form of cell type-specific partial IFN-γR1 deficiency caused by a germ line mutation of the IFNGR1 initiation codon. Human Molecular Genetics, 19 (3): 434-444

Rockefeller University (2010, February 21). Human genetic vulnerabilities may underlie infectious diseases, scientist argues. ScienceDaily

Rockefeller University (2010, January 1). Mutation leads to new and severe form of bacterial disease. ScienceDaily.

University of New South Wales (2008, December 9). Blame Your Genes: Some People Eight Times More Likely To Suffer From Prolonged Illness With Infection. ScienceDaily.

Campylobacter jejuni-Associated Guillain-Barré Syndrome: It’s No Picnic

Student guest post by D.F. Johnston

As the year marches forward, ever closer to that summer sun we missed so much during dreary winter days, we also get closer to the traditional summer picnics and barbecues. Sometimes, in our hurry to enjoy quality time with friends and family, we get distracted from our usual practices for proper food handling. We might try to get little Billy his hamburger before he has time for a full-fledged temper tantrum, so we hurry it along, figuring a tiny bit of pink in the middle won’t be the end of the world. Or we might realize that we’re short a couple of serving spoons and re-use the meat fork for the raw fruit or veggie tray. After all, even if we’re thinking about foodborne illness, a little diarrhea is our biggest worry, right?

Actually, amongst the wide range of microbes that can cause foodborne illness, one of the more common is a Gram-negative bacterium called Campylobacter jejuni, which lives in the intestines (where the name “jejuni” comes from) and it is most often encountered in undercooked poultry or via cross-contamination. This bacterium does cause the well-known symptom of short-term diarrhea and usually resolves on its own over the course of two to ten days or with antibiotic treatment (1). Many people who worry about foodborne illness worry about the well-known salmonellosis or the dreaded E. coli O157:H7. According to the National Center for Zoonotic, Vector-Borne, and Enteric Diseases estimates for the number of cases of shiga-toxin producing E. coli, enterohemorrhagic E. coli, salmonellosis and an Institute of Medicine estimate for enterotoxigenicE. coli, the combined total number of cases occurring each year in the United States is approximately 880,000 (2-5). Ironically, cases of Campylobacter are over 2.5 times more common, as there are approximately 2.4 million cases in the United States each year (6). Campylobacter probably isn’t as infamous as it tends to occur in small clusters like at family picnics, rather than in high-profile outbreaks and recalls.

Unfortunately, discomfort and dehydration are not the only possible consequences of campylobacteriosis. Lindsay mentions temporary arthritis and hemolytic uremic syndrome, which can result in renal failure, as potential consequences of C. jejuni infection (7). Additional chronic conditions associated with prior infection with C. jejuni are mentioned by the Food Research Institute at the University of Wisconsin-Madison and include appendicitis, carditis, Reiter syndrome, and Miller Fisher syndrome, which is a subtype of Guillain-Barré syndrome (8). There are several forms of Guillain-Barré syndrome (GBS), making the range of symptoms wide as well, but some of the more commonly encountered effects are limb and respiratory weakness, and loss of reflexes (9). Several organisms may precipitate GBS, in addition to C. jejuni, such as cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae, although Campylobacter-associated forms may be more severe in clinical presentation (10, 11). Typically, GBS associated with C. jejuni follows 1-3 weeks after infection and patients generally recover within weeks to months (11). However, there is a 2-3% mortality rate and 20% of GBS cases may have significant and lasting neurologic effects (12). Between 30-50% of all GBS cases are linked to C. jejuni infection (12).

Since there are several forms of clinical presentation for GBS, the forms also differ in hypothesized mechanisms for how the disease is caused or what part of the nerve cell is directly affected (i.e. the myelin sheath versus the axon or T-cell mediated versus antibody-mediated) (11). Despite this, the current conception for all types is of GBS being caused by the immune system reacting to an external factor (such as C. jejuni) to the degree that human cells become collateral damage in one form or another. One of the more popular theories is that part of a molecule on the surface of the bacterium is very similar to those found on nerve cells in the human body, leading to an antibody attack on nerve cells even after the Campylobacter has been eliminated. This mechanism is further supported by the other agents suspected in causation of GBS since they also have a similarly-shaped molecule on their surface (11). The paralysis or muscle weakness may occur because the immune system breaks open the protective Schwann cells surrounding the nerves, allowing enzymes to begin breaking down the myelin “insulation” of nerve axons that help ensure reception and speed of nerve impulses (11).

The first causal relationship for C. jejuni and GBS was hypothesized in 1982 based on a case report and similar reports continued after this (11). Isolation and growth of Campylobacter from the stool of GBS patients also supported such a relationship, but was assumed to underestimate bacterial presence, as time from initial infection to culture and culture methodology could strongly influence recovery of the bacterium (11). Lab techniques to detect antibodies to C. jejuni have also been used to demonstrate presence of the organism in GBS patients, although this technique is subject to cross-reaction with closely related bacteria (11). That GBS appears 1-3 weeks after bacterial infection (the time it takes to produce an antibody response) also supports an infectious event leading to GBS. Animal models have strengthened support for the association, as rabbits and mice have been injected with molecules similarly shaped to those of C. jejuni and have developed high titers of antibodies that also react against nerve cells (11, 12). The NIH appears to accept the role of Campylobacter in GBS etiology and has moved to outlining steps for improving mechanistic knowledge (11); the published literature also reflects this general acceptance.

This summer, my family reunion is going to use safe food handling techniques in an attempt to lower my family’s risk for the unpleasantness of campylobacteriosis and the subsequent risk for Guillain-Barré syndrome and other Campylobacter-associated chronic conditions. Have a look at the USDA guidelines for proper food handling and enjoy your summer pursuits (13).

Works Cited

1. Ang, J.Y. & Nachman, S. 2009. “Campylobacter Infections.” eMedicine.

2. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Escherichia coli O157:H7.” Centers for Disease Control and Prevention.

3. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Enterohemorrhagic Escherichia coli: Technical Information.” Centers for Disease Control and Prevention.

4. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Salmonellosis.” Centers for Disease Control and Prevention.

5. Stratton, K.R., Durch, J.S., & Lawrence, R.S (Institute of Medicine). 2000. “Vaccines for the 21st Century: A Tool for Decisionmaking–Appendix 5: Enterotoxigenic E. coli.” National Academies Press.

6. National Center for Zoonotic, Vector-Borne, and Enteric Diseases. 2009. “Campylobacter, General Information.” Centers for Disease Control and Prevention.

7. Lindsay, J.A. 1997. “Chronic Sequelae of Foodborne Disease.” Emerg Infect Dis, 3(4): 443-452. http://www.cdc.gov/ncidod/EID/vol3no4/lindsay.htm

8. Doyle, M.E. 1998. “Campylobacter–Chronic Effects.” UW-FRI Briefings.

9. Davids, H.R. & Oleszek, J.L. 2010. “Guillain-Barré Syndrome.” eMedicine.

10. Yu, R.K., Usuki, S., & Ariga, T. 2006. “Ganglioside Molecular Mimicry and Its Pathological Roles in Guillain-Barré Syndrome and Related Diseases.” Infect Immun, 74(12): 6517-6527.

11. Nachamkin, I., Allos, B.M., & Ho, T. 1998. “Campylobacter Species and Guillain-Barré Syndrome.” Clin Microbiol Rev, 11(3): 555-567.

12. Moore, J.E., Corcoran, D., Dooley, J.S.G., Fanning, S., Lucey, B., Matsuda, M., McDowell, D.A., Megraud, F., Millar, B.C., O’Mahony, R., O’Riordan, L., O’Rourke, M., Rao, J.R., Rooney, P.J., Sails, A., & Whyte, P. 2005. Campylobacter.” Vet Res, 36(3): 351-382.

13. USDA: Food Safety and Inspection Service. 2010. “Safe Food Handling Fact Sheets.”

Image from: http://en.wikipedia.org/wiki/Campylobacter

Psychological Disorders Associated with Cerebral Malaria

Student guest post by Laura Vonnahme

As a part of traveling to a developing nation, we are often required to take medical precautions. This generally includes a line-up of shots for various diseases, a few other tests, and various regimens of prophylaxis for possible diseases. I have often left these doctors appointments with a line of band-aids on my arm, a handful of prescriptions and a little weakness in my knees. However, I will readily admit that my malaria prophylaxis is often pushed to the back burner; in fact the last time I went to a developing nation, I didn’t even get the malaria prophylaxis until I was in the country and I didn’t even bother taking it for the prescribed amount of time. However, as I readily admit my shortsightedness in the past, I have become more aware of the chronic conditions that can be caused by a single malaria infection.

Malaria is a mosquito-borne disease caused by a parasite, and there are four different species of parasites that cause malaria, Plasmodium falciparum (which is the most fatal), P. vivax, P. malariae, and P. ovale. When initially infected, parasites first enter the liver, then multiply quickly and enter the bloodstream, where they continue to multiply and rupture blood cells2. While P. falciparum causes the most severe symptoms, P. vivax and P. ovale can cause chronic malaria which is characterized by profound anemia, enlargement of the spleen, emaciation, mental depression, sallow complexion, edema of ankles, feeble digestion, and muscular weakness.

In addition, there is a more serious form of malaria caused by P. falciparum, called cerebral malaria, which can be deadly quickly if left untreated. However, a more controversial disease has been linked to malaria as of late. Recently there have been links to cerebral malaria, posttraumatic stress disorder (PTSD) and other psychological disorders in soldiers who have returned from service in areas where malaria is endemic. In particular several studies have been conducted on soldiers who had contracted malaria while in service during the Vietnam War. Dr. Nils R. Varney conducted one of these first studies here at the University of Iowa and reported that many cerebral malaria survivors from the Vietnam War have a number of neuropsychiatric symptoms that can persist for years after the acute illness has been treated. “Cerebral malaria does a number of different things to a patient’s brain that cause a variety of neurological problems,” Varney says. “…patients who survived the illness frequently developed depression, impaired memory loss, personality change and proneness to violence as long-term effects of the disease. These are symptoms that have been reported by many Vietnam veterans for years and are often treated strictly as PTSD.”

The journal article compared the neuropsychiatric status of 40 Vietnam combat veterans who contracted cerebral malaria between 1966-1969 with 40 Vietnam veterans with similar wartime experience who suffered gunshot or shrapnel wounds during the same period. The participants underwent numerous tests for sensory, cognitive and behavioral symptoms. Findings indicate that cerebral malaria results in multiple, major, substantially underappreciated neuropsychiatric symptoms in Vietnam veterans, including poor dichotic listening, “personality change,” depression, and, in some cases, partial seizure-like symptoms. Findings strongly suggest that history of malaria should be considered in any medical, psychological, or psychiatric workup of a Vietnam War veteran because a positive response could result in substantial changes in diagnosis and treatment. Interestingly, these results seen in Vietnam veterans are similar to those seen in British troops stationed in India during in the 19th century during the height of the British Empire. Nineteenth-century physicians documented these cases and considered malaria a leading cause of mental illness in British-occupied regions

Therefore, continued prophylaxis is extremely important for anyone traveling to an area where malaria is thought to be endemic. Thus, while you may think prophylaxis is a nuisance, the pills make you have weird dreams, you cant remember to take the pill every week or you just plain think your invincible, none of these are valid excuses for skipping a necessary malaria prophylaxis.


1. CDC – Malaria. (n.d.). Centers for Disease Control and Prevention. Retrieved April 11, 2010, from http://www.cdc.gov/malaria/

2. Malaria. (n.d.). Penn State Hershey. Retrieved April 11, 2010, from http://www.hmc.psu.edu/healthinfo/m/malaria.htm

3. UI/VAMC study says patient’s history of malaria may be a clue to many Vietnam vets’ psychological and other health problems. (n.d.). Retrieved April 11, 2010, from http://www.newswise.com/articles/uivamc-study-says-patients-history-of-malaria-may-be-a-clue-to-many-vietnam-vets-psychological-and-other-health-problems

4. Varney, N., Roberts, R., & Springer, J. (1997). Neuropsychiatric Sequelae of Cerebral Malaria in Vietnam Veterans. The Journal of Nervous & Mental Disease, 185(11), 695-703. Retrieved April 11, 2010, from http://journals.lww.com/jonmd/Abstract/1997/11000/Neuropsychiatric_Sequelae_of_Cerebral_Malaria_in.8.aspx

The Complex Etiology of Celiac Disease Includes Gluten, Pathogens, Predisposed Host Microflora and Immune Response

Student guest post by Ahn To

There are two separate philosophies regarding the relationship between life and food. There are those that believe we only eat to live. On the other hand, there are those that believe one of life’s greatest pleasures is food. I am a firm believer of the latter, thus, you can imagine my horror when I first learned of celiac disease (CD). This is a disease with no treatment except for a lifetime on a gluten-free diet, thus people with CD cannot eat many types of food. I knew then that I had to find out more about causation of CD, which includes the complex interaction between genes, “gluten”, immune response, microflora and infections.

CD has both genetic and environmental contributing factors. Genetic factors, being homozygous or heterozygous for HLA-DQ2 or HLA-DQ8 genes, which are coded for class II antigen presenting cells in the immune system, confer susceptibility to CD. However, these genes are much more common than the number of people with CD, thus there may be other genetic contributions. Future studies are needed to identify them. Environmental factors, proline- and glutamine-rich proteins (widely known as gluten) are believed to be the trigger of the diseases. There is also evidence that infections may have a role in CD etiology.

CD is an autoimmune disease. In an infection, the immune cells target non-self antigens on the pathogens. Once the pathogens are eradicated, the immune system becomes deactivated. As the immune system fights the pathogen, it may damage some tissue, but that is not a problem since the body has an innate capacity to heal itself. In an autoimmune reaction, the antigens that the immune system target cannot be completely eradicated because they are self antigens, and so the fight doesn’t end. As time passes, the body’s capacity to heal cannot keep up, which results in severe damage to the body. The underlying causation of an autoimmune disease is the immune system’s failure to differentiate between self and non-self antigens.

There are several hypotheses regarding infection roles in CD. One of which is “molecular mimicry”. This theory proposes that there are antigens on pathogens that are similar enough to host antigens that after the immune system cleared the pathogens’ antigens, it mistakes the host antigens as pathogenic and starts to attack the host antigens. Another theory proposes that infections alter intestinal permeability, which allows “gluten” peptides to encounter HLA-QB, which lead to tissue damages through an influx of “gluten”-specific T cells. In CD, the immune system causes villous atrophy and crypt cell hypertrophy, which result in malabsorption of nutrients.

An association between being born in the summer and having an increased risk for CD was discovered in 2003 through analyzing data from a population based registry of celiac disease in Sweden. The reason for this was speculated to be a higher rate of infection and easier food spoilage in the summer. Thus a child born in the summer has a higher risk of getting an infection that can contribute to CD pathogenesis. Along the same line of reasoning, there was a review in 2009 that indicated that perinatal infections and maternal-milk may have a protective role in CD development. That same review also linked CD to Adenovirus 12 or Hepatitis C virus. Rotavirus infection was also linked to CD in a prospective cohort study of 1,931 children in the Denver metropolitan areas. That study also found that repeated infections of Rotavirus correlate to a higher risk than single infection. However, not all infections increase the risk of having CD. In a retrospective serological case-control study, Leeor Plot et al. found that having past infection of Rubella, CMV or EBV actually has a protective effect leading to a decrease in the risk of having CD. This indicates that pathogenic infections are only a part of the story.

A case-control by Tjellstrom et al. indicates that there is a difference in the metabolic activity of intestinal microbial flora in CD patients. Thus, it is reasonable to propose that it is an interaction between microflora, infectious agents, gluten and the immune system in a genetically predisposed person that causes CD.

Having CD doesn’t mean you have to stop enjoying food. As I talked to people with CD, who are on a gluten free diet, they referred me to many websites dedicated to gluten-free cooking. These websites not only have gluten free recipes for daily meals, but also yummy desserts like cookies and cakes. If you are looking for a wheat substitute, you should check out rice. There are around 40,000 different kinds of rice to choose from. Moreover, since Asian food has a strong emphasis on rice instead of wheat, you can find many delicious ethnic dishes that are gluten-free: rice and chicken curry from India, pho from Vietnam, papaya salad from Thailand… Of course, you can still eat out, since many restaurants have a list of which dishes are gluten-free or you can specifically request gluten-free dishes. So it is possible to enjoy good food when one has CD. However, I hope that future research can modify the interaction between gluten, pathogens, host microflora and immune response in genetically predisposed individuals to prevent the onset of CD, so people can eat whatever they want.


1. Ivarsson A, Hernell O, Stenlund H, Persson LA. Breast-feeding protects against celiac disease. Am J Clin Nutr 2002;75:914-921.
2. Kagnoff MF. Celiac disease: pathogenesis of a model immunogenetic disease. J Clin Invest. 2007;117:41-49.
3. Plot L, Amital H. Infectious associations of Celiac disease. Autoimmun Rev. 2009;8:316-319.
4. Plot L, Amital H, et al. Infections May Have a Protective Role in the Etiopathogenesis of Celiac Disease. Contemporary Challenges in Autoimmunity 2009: Ann. N.Y. Acad. SCi. 1173:670-374.
5. Stene, LC, Honeyman, MC, Hoffenberg, EJ, et al. Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: A longitudinal study. Am J Gastroenterol 2006;101:2333-2340.
6. Tjellstrom, B., Stenhammar, L., Hogberg, L., Falth-Magnusson, K., Magnusson, K. E., Midtvedt, T., Sundqvist, T. & Norin, E. (2005). Gut microflora associated characteristics in children with coeliac disease. Am J Gastroenterol 100, 2784-2788.


Student guest post by Francis Mawanda.

HIV/AIDS is a major public health problem worldwide. To date, it is estimated that more than 60 million people have been infected with HIV and more than 25 million people have died as a result of HIV/AIDS worldwide1. Despite the high prevalence and mortality rates that are associated with HIV/AIDS, and after more than 29 years of aggressive research efforts, there is still no cure or vaccine to prevent against HIV/AIDS. And although the introduction of antiretroviral (ARV) drugs in the mid 1990s greatly improved the outlook, health and quality of life of people living with HIV/AIDS, ARV drugs are associated with issues of viral resistance, serious side effects and high costs which render them unavailable in developing countries with the greatest HIV/AIDS burden. Therefore, prevention remains the key in the fight against HIV/AIDS.

Since the beginning of the HIV/AIDS epidemic, prevention has always been recognized as the major method for controlling the spread of HIV/AIDS. As a result, numerous HIV/AIDS prevention programs have been implemented in countries and communities all over the world. While these programs initially succeeded in reducing the prevalence of HIV/AIDS, current trends suggest that after an initial decline HIV/AIDS prevalence in most countries has plateaued over the last decade1 with new infections still being diagnosed every day. According to UNAIDS & WHO, in 2008 alone there were more than 2.7 million new cases of HIV/AIDS worldwide1 representing an average of 7000 new cases per day.

The continued spread of HIV/AIDS despite aggressive prevention programs and widespread public awareness presents a public health dilemma. This is true not only for HIV/AIDS, but for most health conditions that are associated with behavioral and or lifestyle risk factors such as smoking and lung cancer. This is because the reasons why people continue to engage in high risk behavior despite awareness of the possible negative health consequences are multiple, complex, and not only vary from individual to individual, but even for each individual, the reasons may vary from situation to situation or from one environment to another.

However, given that HIV can only be transmitted to an uninfected person from an infected person, then the continued spread of HIV/AIDS could be attributed in part to the fact that majority of current HIV/AIDS prevention programs are aimed at increasing awareness and reducing high risk sexual behavior among HIV negative individuals. These programs not only ignore the role people living with HIV/AIDS play in the HIV transmission equation, but also assume that people living with HIV/AIDS do not engage in high risk sexual behavior. However, recent studies have shown that a significant proportion of people living with HIV/AIDS continue to engage in high risk sexual behavior even after diagnosis of HIV/AIDS2,3,4. Therefore, there is a need for prevention programs aimed at increasing awareness and reducing high risk sexual behavior among people living with HIV/AIDS as well.

However, in developing and implementing HIV/AIDS prevention programs that target people living with HIV/AIDS, the fact that the population of people living with HIV/AIDS consists of individuals with HIV/AIDS and are aware of their HIV serostatus and individuals with HIV/AIDS but are unaware of their HIV serostatus should be considered since both groups require different approaches and yet both groups should be targeted concurrently in order for prevention efforts to succeed.

A large number of people living with HIV/AIDS, especially in developing countries are unaware of their HIV serostatus. These individuals continue to spread HIV/AIDS to their partners unknowingly. The huge role this group of individuals plays in the spread of HIV/AIDS has recently been recognized and as a result some countries have implemented programs to encourage people to test for HIV/AIDS and in some countries such as Botswana, by making HIV testing part of routine medical care. However these efforts alone without efforts targeted at people living with HIV/AIDS who are aware of their serostatus would be ineffective not only because routine testing does not involve proper HIV/AIDS counseling but also because as noted above some individuals will continue to engage in high risk sexual behavior after receipt of a positive HIV serology test . In addition, because HIV prevention is one of the major factors motivating individuals from engaging in high risk sexual behavior, after an HIV diagnosis there is no longer motivation not to engage in high risk sexual behavior except as an act of altruism.

In terms of people living with HIV/AIDS and who are aware of their HIV/AIDS serostatus, some governments have also recognized the role of this group of people living with HIV/AIDS in the continued spread of HIV/AIDS and as a result some countries have taken steps to prevent these individuals from spreading HIV/AIDS. These include laws and sentences for people living with HIV/AIDS and are aware of their serostatus who transmit HIV to an uninfected individual. However such efforts alone are also ineffective as they may instead discourage individuals from testing for HIV/AIDS to prevent prosecution and yet these programs depend on well documented and widespread HIV serostatus awareness. In addition, these programs are not practical in developing countries with the highest HIV/AIDS burden, simply because medical record keeping is inadequate making it very difficult to determine an individuals’ serostatus prior to any alleged contact.

However a combination of programs aimed at people living with HIV/AIDS who are unaware of their serostatus such as routine HIV/AIDS testing and proper counseling with programs aimed at people living with HIV/AIDS who are aware of their serostatus such laws and prosecution would address most of the issues that arise from targeting only one group.

Therefore there is not only a need for increased programs aimed at HIV/AIDS prevention through people living with HIV/AIDS but these programs should target both people living with HIV/AIDS and are aware of their HIV serostatus and people living with HIV/AIDS who are unaware of their HIV serostatus in addition to the programs aimed at people without HIV/AIDS. This would ensure that everyone regardless of their serostatus is involved in stopping the continued spread of HIV/AIDS.

1. UNAIDS, WHO (2009). 2008 report on the global HIV/AIDS epidemic. Available from http://www.unaids.org/en/KnowledgeCentre/HIVData/GlobalReport/2008/2008_Global_report.asp

2. Heckman T, Kelly J, Somiai A. Predictors of continued high-risk sexual behavior in a community sample of persons living with HIV/AIDS. AIDS and Behavior. 1998; 2: 127-135.

3. Kalichman S. Psychological and social correlates of high risk sexual behavior among men and women living with HIV/AIDS. AIDS Care. 1999; 11: 415-428.

4. Reilly T, Woo G. Predictors of high-risk sexual behavior among people living with HIV/AIDS. AIDS and Behavior. 2001; 5(3): 205-217.