infection prevention

Immunological Responses to Bacterial and Viral Infections

Most people can avoid infection progression by activating their immune systems. Furthermore, immunological deficits are linked to an increased susceptibility to infections. I examine immunological responses to bacterial and viral illnesses in this essay.

Immune Response to Bacterial Infections

As bacteria infect the body, the immune system responds in one of three ways: complement mediated lysis, phagocyte mediated lysis, and phagocyte mediated lysis. Phagocytosis, also known as cell-mediated lysis.

Complement Mediated Lysis

When bacteria are attacked by complement proteins, lysis occurs, as illustrated by (Stefan H. E. Kaufmann, 2010). These immune proteins kill bacteria by three different pathways: the lectin pathway, the classical complement pathway, and the alternative pathway. The classical complement pathway involves antibodies binding to the target bacterium’s surface. According to (J.G. Sissons, 2012), these antibodies are then targeted by complement protein complex C1 which then bind to the antibody’s Fc region. After binding, the C1 initiates a series of cleavage and reforming of complement complexes culminating in the formation of a membrane attack complex. The C1 can also produce opsonin that marks the bacteria for destruction. The membrane attack complex can only insert into cell membranes of gram-negative bacteria, where it causes porosity, allowing access to membrane damaging molecules making the cell prone to osmotic lysis. In the alternative complement pathway, complement proteins form a C3 complex which binds directly to bacteria activating downstream components and again leading to membrane attack complex formation and subsequent lysis. The lectin pathway uses mannan binding lectin that binds to proteins with mannose residues forming a complex with MBL activated serine protease or MASP. The MASP cleaves C2 and C4 activating C3 convertase that then takes part in Membrane attack complex formation.

Phagocyte Mediated Lysis

The immune system can also respond to bacteria by initiating phagocytosis. Through opsonization, immune proteins bind onto the bacteria’s surface making the bacteria recognizable to phagocytic cells, which then engulf and destroy bacteria. Gram-positive bacteria, which are resistant to membrane attack complex, are destroyed through opsonization (J.G. Sissons, 2012). After phagocytosis, bacteria are broken down into smaller fragments which are presented on the phagocytes’ surface by class II major histocompatibility molecules. Th1 and Th2, the major circulating helper T cells, produce cytokines after identifying the bacterial fragments. Th1 cells secrete Interferon-g which causes cell-mediated mechanisms while Th2 cells mostly secrete interleukin-4 that activates B cells, promoting humoral immunity. B cells secrete antibodies into body fluids.

Cell Mediated Immunity

Cell-mediated immunity occurs when bacteria undergo phagocytosis but do not get destroyed and survive inside the cells. These intracellular bacteria mostly target macrophages. Antigen presentation then occurs where bacterial peptides are presented on the surface of infected macrophages via MHC class II molecules. (Stefan H. E. Kaufmann, 2010) adds that on detection of bacterial peptides, Th1 cells then secrete Interferon-g that in turn stimulates mechanisms that digest and destroy the bacteria within the cell. The bacteria are also made more visible by interferon-g, which increases antigen presentation by cells, making them more susceptible to destruction.

Body’s Response to Viral Infections

Unlike bacterial infections, most viral infections are intracellular. The body controls these infections with macrophages, natural killer cells, and interferons type I. The type I interferons are produced by cells infected with the virus. Interferon gamma triggers macrophages that destroy the virus as explained by (B.A. Askonas, 2012). It also activates natural killer cells that secrete perforin and granzyme, which also destroy the infected cells. Correspondingly, interleukin-12, which is produced by antigen-presenting cells and macrophages, causes the natural killer cells to increase cytotoxicity, thereby producing more interferon-g, which sequentially causes increased microbicide potential of macrophages. Interferons also prevent the virus from replicating within a cell.

TCD8+ Cells Activation

TCD8+ cells activation occurs in adaptive immunity. They exert cytotoxicity through MHC class I causing the release of perforin and granzyme that subsequently cause lysis of infected cells. In addition, activation of TCD4+ cells occurs, and they work together with B cells yielding antibodies (Stefan H. E. Kaufmann, 2010). The antibodies work on a virus extracellularly before it infects another cell. They bind to the virus and neutralize it such that it cannot infect another cell. In contrast, antibodies can promote cellular toxicity mechanisms, permitting action by natural killer cells. In some viral infections, antibodies can protect the body of a previously sensitized host by intercepting the virus. In most viral infections, destruction of infected cells involves several mechanisms.

References

B.A. Askonas, B. M. (2012). The Immune Response to Viral Infections. Springer Science & Business Medi.

J.G. Sissons, L. B. (2012). Immunology of Infection. Springer Science & Business Media.

Stefan H. E. Kaufmann, B. T. (2010). The Immune Response to Infection. American Society for Microbiology Press.