Block 9 Micro Viral Immunology

NK cells are the most likely to be responsible for killing infected cells that express very low levels of MHC-I. NK cells have the ability to recognize and kill cells that have reduced or absent MHC-I expression, which is a common evasion strategy used by viruses. NK cells have specific receptors that can detect these changes in MHC-I expression and initiate a cytotoxic response to eliminate the infected cells. This allows the immune system to still control viral populations even in the absence of CD8+ T lymphocyte-mediated cytotoxicity.

The correct answer is Capsid. The capsid is the protein coat that surrounds the RNA genome of a virus. In the case of a naked, (+) ssRNA virus, the capsid is the structure that serves as the target for neutralizing antibodies. These antibodies bind to the capsid and prevent the virus from infecting host cells. The RNA, lipid bilayer, envelope glycoprotein, and RNA polymerase are not the primary targets for neutralizing antibodies in this specific scenario.

Cell-mediated (CD8+) cytotoxicity and IFN-a secretion are the most important hallmarks of antiviral defense. Cell-mediated cytotoxicity refers to the ability of CD8+ T cells to recognize and kill virus-infected cells, thereby preventing viral replication and spread. IFN-a secretion, on the other hand, is a type of interferon that plays a crucial role in activating immune cells and enhancing their antiviral activity. This combination of cell-mediated cytotoxicity and IFN-a secretion helps to eliminate virus-infected cells and control the spread of the virus within the body.

The TH1 response is characterized by the production of IFN-y and IL-12. These cytokines play a crucial role in activating macrophages and cytotoxic T cells, which are important for eliminating viral infections. IFN-y stimulates the production of antiviral proteins and enhances the killing ability of cytotoxic T cells, while IL-12 promotes the differentiation of TH1 cells and enhances their ability to produce IFN-y. Therefore, the presence of IFN-y and IL-12 is indicative of a strong TH1 response in host defense against viral infections.

The expression of the genes encoding Pkr, 2',5'-oligo(A) synthetase, and RNase L is primarily under the control of the Jak/STAT signaling pathway.

MHC-I restricted antigen presentation is important for viral clearance because it is the main pathway through which virus-infected cells are killed. MHC-I molecules present viral antigens on the surface of infected cells, allowing cytotoxic T cells to recognize and destroy these cells. This is a crucial mechanism in the immune response against viral infections, as it helps to eliminate the source of the virus and prevent its spread to other cells.

Neutralizing antibodies target the envelope glycoprotein of enveloped, (-) ssRNA viruses. The envelope glycoprotein is located on the surface of the virus and plays a crucial role in viral entry and infection. By targeting this protein, neutralizing antibodies can prevent the virus from attaching to host cells and entering them, thereby neutralizing the virus and preventing infection.

IFN-a exerts its antiviral activity through the synthesis of Pkr protein. Pkr protein is an enzyme that is activated in response to viral infection. Once activated, Pkr protein inhibits protein synthesis in infected cells, preventing the virus from replicating and spreading. This helps to control the viral infection and limit its impact on the host.

IFN-a increases the expression of inactive RNA-activated protein kinase (Pkr) which, when activated by double-stranded RNA, inactivates the translation activator eIF2. This leads to the termination of mRNA translation and promotes apoptosis and autophagy.

Macrophages play a crucial role in orchestrating the CD8+ T lymphocyte cytotoxicity response. They act as antigen-presenting cells, presenting viral antigens to CD8+ T cells to initiate their activation and cytotoxicity. Macrophages also produce cytokines and chemokines that attract and activate CD8+ T cells. Therefore, they are essential for coordinating the immune response against viral infections.

Virus neutralization is not an innate host defense mechanism because it is primarily a function of the adaptive immune system. Innate host defense mechanisms are the body's first line of defense against pathogens and are present from birth. These mechanisms include apoptosis, IFN-a secretion, alternative activation of the complement pathway, and autophagy. Virus neutralization, on the other hand, involves the production of specific antibodies by B cells in response to a viral infection, which is a characteristic of the adaptive immune response.

Interferon-α (IFN-α) treatment for hepatitis B works by decreasing mRNA translation in virally-infected cells through the up-regulation of Pkr. This means that IFN-α increases the activity of Pkr, which in turn inhibits the translation of viral mRNA, ultimately reducing viral protein synthesis. By decreasing viral protein production, IFN-α helps to suppress the replication and spread of the hepatitis B virus in the patient's body.

IFN-y, also known as interferon-gamma, is responsible for the non-cytolytic purging of virally-infected cells by CD8+ T lymphocytes. This cytokine activates macrophages and enhances their ability to eliminate intracellular pathogens, including viruses. It also promotes the production of antibodies and increases the expression of MHC molecules, aiding in the recognition and clearance of infected cells. Therefore, IFN-y plays a crucial role in the immune response against viral infections by CD8+ T lymphocytes.

Toll-like receptors are a class of proteins that play a key role in the innate immune response. They recognize specific patterns on pathogens, including viruses, and initiate a signaling cascade that leads to the expression of type I interferons (IFNs). These IFNs are important in the antiviral response, activating various immune cells and promoting the production of antiviral proteins. Therefore, the most likely receptor that will initiate the cascade leading to type I IFN expression in virus-infected cells is the Toll-like receptor.

RIG-1 is the most likely receptor that will initiate the cascade leading to type I IFN expression in virus-infected cells. RIG-1 is a pattern recognition receptor (PRR) that recognizes viral RNA and activates the innate immune response. Upon binding to viral RNA, RIG-1 triggers a signaling cascade that leads to the production of type I interferons, which are key molecules in antiviral defense. Therefore, RIG-1 is the most likely receptor involved in initiating the cascade leading to type I IFN expression in virus-infected cells.