Co-infections are sometimes fatal: Here is the answer to the Q why

Your immune system is your body's defense against infections and other harmful invaders. Without it, illnesses from bacteria, viruses  and other micro-organisms would be constant.

Your immune system is made up of special cells, tissues, and organs that work together to protect you.

When your immune system doesn't work the way it should, it is called an immune system or immunodeficiency disorder. You may be born with a weak immune system. This is called primary immune deficiency. You might get a disease that weakens your immune system. This is called acquired immune deficiency. You can have an immune system that is too active or have an immune system that turns against you. Conditions called autoimmune disease occur.

Acquired immune deficiencies. Your  immune system can be weakened by certain drugs, for example. This can happen to people on chemotherapy or other drugs used to treat cancer, or to people following organ transplants who take medication to prevent organ rejection. Also, infections like the flu virus, mononucleosis (mono), and measles can weaken the immune system for a brief time. Your immune system can also be weakened by smoking, alcohol, and poor nutrition. HIV, which causes AIDS, is an acquired viral infection that destroys important white blood cells and weakens the immune system. People with HIV/AIDS become seriously ill with infections that most people can fight off. These infections are called "opportunistic infections" because they take advantage of weak immune systems.

When people have compromised immune systems that are vital to fight diseases because of an infection, other infections could prove fatal. When patients have multiple infections, this leads to more debilitating symptoms, intractable cases, and complicated presentations for a physician to diagnose.

Lyme disease is another example. One tick often carries more than one disease, so it is not uncommon for people to get more than one infection from the bite of a single tick, resulting in deadly co-infections along with Lyme disease. Treatment becomes more complicated when co-infections are involved, and there is an increased rate of relapsing. If co-infections are left untreated, it will escalate into a serious health-threat, and the patient will become increasingly ill. Lyme disease is an immuno-suppressant (it severely lowers your immune response) and although rare, can be fatal.

Swine flu is one more example which is the cause of deaths in people who get infected with other microbes too.

My father had died because of co-infections too. He had hepatitis which led to a weak immune system because he was not treated ( he didn't tell us in the first place that he was suffering) and bacterial co-infections led to septicemia and his death by the time we ourselves realized his condition. That is one of my greatest regrets in life. Being a microbiologist, I couldn't save my father from these deadly infections.

Now researchers have found the root cause of this compromised immune system in case of malaria and viral co-infections.

Acute infection with the mouse equivalent of Epstein Barr virus (EBV) reduces the immune response to malaria-causing Plasmodium infection, resulting in normally non-lethal Plasmodium yoelii XNL infection becoming lethal in mice. This is one of the findings of a new paper in the journal PLoS Pathogens from a team of researchers led by Tracey Lamb and Samuel Speck, both from Emory University, Atlanta, USA. The results are potentially important in the context of infection control initiatives in sub-Saharan Africa, where many children become infected with EBV by the age of six months. The results of this paper suggest that this EBV infection could contribute to reduced immune responses to malaria-causing parasites and help explain why some children cannot acquire immunity to severe non-cerebral malaria, as would normally be expected after 1-2 infections.

EBV is a gammaherpesvirus which infects B cells, the antibody- producing cells of the immune system. After an asymptomatic acute infection phase of approximately four weeks, the infection remains latent throughout the lifetime of the host. It is well established that children infected with both EBV and with the malaria parasite Plasmodium falciparum (P. falciparum) have reduced immunity to EBV and are susceptible to development of the EBV-associated jaw tumour, endemic Burkitt’s lymphoma, the most lethal childhood cancer in equatorial Africa, with highest prevalence in the 5-9 year old age group. However, despite this recognised link between co-infection with EBV and P. falciparum on EBV immunity, it was not known whether there was also an impact on immunity to P. falciparum.

In the current study, the research team used a mouse model of infection with murine gammaherpesvirus 68 (MHV68), the mouse equivalent of EBV. They co-infected the mice with one of two well-established non-lethal strains of mouse Plasmodium parasites, namely P. yoelii XNL and P. chabaudi AS. The results of the study showed that acute but not latent infection with EBV reduced the anti-malarial humoral (antibody) response to both strains. As a result, the normally non-lethal P. yoelii infection became lethal. The P. chabaudi infection has been previously shown to be more independent of antibody-mediated immune responses and did not become lethal.

The research team examined the basis of the loss of immunity against P. yoelii during acute MHV68 infection and found that a subset of anti-parasite immune T cells in the spleen, called T follicular helper cells, was not maintained. This in turn meant that parasite- specific B cells (precursors of antibody-producing plasma cells) were also lost, resulting in insufficient plasma cells making anti- Plasmodium antibodies. The team further established that a viral protein called MHV68-derived latency associated protein M2 is essential for the failure in the co-infected mice to launch an anti-Plasmodium humoral respose and that in the mouse model this effect lasted for 30 days, during the acute phase of infection. If the M2 protein was removed from P. yoelii, infections were not lethal in the virally co-infected mice.

The research team concluded that their work provides compelling evidence that acute gammaherpesvirus infection can negatively modulate the humoral immune response to malaria infection. Currently, few human studies exist in which a link between EBV infection and malaria infection has been considered and there are no large epidemiological studies. The authors of this study suggest that their results are consistent with the limited existing evidence suggesting that EBV infection can compromise immune responses to secondary pathogens. They suggest that this justifies investigation of how EBV infection might impact the development of P. falciparum humoral immunity in young children living in malaria endemic areas.

Research source: http://journals.plos.org/plospathogens/article?id=10.1371/journal.p...