Viral Effects on our Immune System

Viruses have the capability to take advantage of our own immune system and use our own cells to produce copies of itself. In this sense, viruses can be extremely deadly to the cells and eventually even lethal to the organism itself. They infiltrate cells by the receptors on their outer protein code and bind to the membrane of cells. Once they enter the cell, they use the cell’s own protein builders and DNA replication methods to produce copies of itself until the cell actually lyses where the viral copies can infect other cells and repeat the process.

Visual representations of 2 different virus types. The influenza has protruding proteins that bind to the membranes of cells. The bacteriophage injects it’s genetic material within the bacteria.

Viruses can even have long term effects on the immune systems of eukaryotes. It can effect both the humoral and cellular immunity of an organism (Notkins 1970). Mice born with a virus were found to have more difficulty producing antibodies. In fact, in some cells the productivity was decreased by as much as 99%. Without antibodies the response rate to infection is greatly decreased, giving the virus more time to infect and spread. In fact, in a similar experiment conducted with mice, when they were injected with a viral gene during their developmental stages, they showed no immunity to that virus when reintroduced to it later in life (Oldstone 1991). This is noteworthy, as vaccines, which are used to cure viruses, are essentially weakened forms of the virus.

In eukaryotes such as plants, it has been found that an adaptation to combat this viral method of infection is through ‘RNA Silencing’ (Voinnet 2001). RNA silencing is where translation is controlled and gene expression is stopped. When DNA is read/proofread, and it notices the foreign genetic material, RNA silencing occurs and makes sure the proteins are not produced. They “block” the transcript through methylation.  And yet, some viruses have shown an alternate adaptation that allows them to greatly decrease the levels of “killer cells” that target the virus (Stern-Ginossar 2007). The virus deregulates the production of ligands, during infection, that helps bind natural killer cells that target virus-infected cells. These killer cells destroy infected cells before they have the chance to “explode” with viral copies and infect other cells. Putting a crutch on this mechanism greatly weakens our immune system response.

One of the deadliest viruses out there is the HIV/AIDS virus. The reason it is so deadly is because it targets and attacks our immune system, making it weaker, thus giving more power and time to the virus to grow and multiply. Now, many cells in the human body have specific surface proteins that will only allow certain molecules to pass through. The surface protein T4, expressed in both the brain and lymphoid cells, has been found to relate with the deadliness of HIV/AIDS (Maddon 1986). The virus, once bound to the T4 surface protein, internalized the information of the T4 in order to easily enter cells in the lymphatic system and the brain, areas where the current virus are heavily located/targeted. This is how the virus “learned” and became such a deadly force. It used our own information against us.

                                                                       Sources                                                                      

Notkins, A. L., S. E. Mergenhagen, and R. J. Howard. “Effect of Virus Infections on the Function of the Immune System.” Annual Review of Microbiology Annu. Rev. Microbiol. 24.1 (1970): 525-38.

Oldstone, M.b.a. “Virus Infection Triggers Insulin-dependent Diabetes Mellitus in a Transgenic Model: Role of Anti-self (virus) Immune Response.” Trends in Genetics 7.7 (1991): 205.

Voinnet, O. “RNA Silencing as a Plant Immune System against Viruses.” Trends in Genetics 17.8 (2001): 449-59.

Stern-Ginossar, N., N. Elefant, A. Zimmermann, D. G. Wolf, N. Saleh, M. Biton, E. Horwitz, Z. Prokocimer, M. Prichard, G. Hahn, D. Goldman-Wohl, C. Greenfield, S. Yagel, H. Hengel, Y. Altuvia, H. Margalit, and O. Mandelboim. “Host Immune System Gene Targeting by a Viral MiRNA.” Science 317.5836 (2007): 376-81.

Maddon, Paul Jay, Angus G. Dalgleish, J.steven Mcdougal, Paul R. Clapham, Robin A. Weiss, and Richard Axel. “The T4 Gene Encodes the AIDS Virus Receptor and Is Expressed in the Immune System and the Brain.” Cell47.3 (1986): 333-48.