Block 9 Micro Viral Pathogenesis

Virally-encoded proteins that increase cell cycling would favor viral replication because they promote the cell cycle progression, leading to increased cell division and proliferation. This provides more host cells for the virus to infect and replicate within, enhancing viral replication.

Adenovirus E3-gp19K inhibits MHC-I transport to the cell surface. MHC-I molecules are responsible for presenting antigens to CD8+ cells, which are cytotoxic T cells. Therefore, the host defense mechanism affected by E3-gp19K is somatic cell-mediated antigen presentation to activated CD8+ cells. This inhibition hinders the ability of CD8+ cells to recognize and eliminate virus-infected cells, allowing the virus to evade the immune response.

The given answer is correct because it states that "Virokines are antiviral host molecules." This means that virokines are molecules produced by the host that have antiviral properties. The other statements in the question are either unrelated to the concept of virokines or are not true. Retroviral gp41 (TM protein) actually increases HIV virulence, some viruses do incorporate host-cell surface proteins, pustules can be a way to spread infection, and RNA-dependent RNA polymerase is prone to error but it is not specifically mentioned as a cause for increased virulence.

This virulence mechanism involves altering the host's defense mechanisms. This means that the virus is able to manipulate or impair the immune response of the host, making it easier for the virus to establish infection and evade elimination by the immune system. By weakening the host's defense mechanisms, the virus can effectively increase its ability to replicate and spread within the host's body.

Virokine is the best term to describe this molecule. The term "viro" suggests that it is related to viruses, and "kine" indicates that it is a signaling molecule. Therefore, virokine refers to a molecule produced by viruses that can modulate the immune response of the host. This term accurately describes the function and origin of the molecule.

Antigenic drift would most likely be involved in viral spread in the human population. Antigenic drift refers to the gradual accumulation of small genetic changes or mutations in the viral genome over time. These changes can lead to the production of slightly different viral strains that may not be recognized by the immune system, allowing the virus to evade immune responses and spread more easily within the population.

Rotavirus NSP4 protein expression is an example of a virulence mechanism that contributes to disease due to the production of a toxin. This suggests that the NSP4 protein produced by rotavirus plays a role in the pathogenesis of the viral infection by causing toxicity in the host.

The presence of high-grade squamous intraepithelial lesions (HSILs) on the cervix, along with the detection of Human papillomavirus type 16 (HPV-16) in the cervical epithelial cells, indicates that the patient has an HPV infection. The HPV-16 protein E7 inhibits cyclin-dependent kinase inhibitors, which leads to an alteration in the cell cycle. This alteration in the cell cycle allows the HPV virus to replicate and persist within the cervical epithelial cells, leading to the development of HSILs. Therefore, the pathophysiological mechanism in this case is the alteration of viral replication or of the cell cycle.

The factors mentioned, suppression of Pkr- and 2’,5’ OAS/RNase L-mediated apoptosis, benefit the hepatitis C virus by preventing the infected cells from undergoing programmed cell death. This allows the virus to persist and replicate within the cells without being eliminated by the immune system. Apoptosis is a natural defense mechanism of the body to remove infected cells, but the virus interferes with this process, enabling its survival and continued infection.

Cytolysis due to viral release refers to the direct destruction of cells caused by the release of viruses from infected cells. When viruses replicate inside host cells, they eventually burst and release new virus particles, leading to the destruction of the infected cells. This mode of tissue damage is considered the most direct because it occurs as a result of the virus itself and not due to the immune response.

The successful infection of a host does not necessarily require terminally differentiated cells. Many viruses can infect a wide range of cell types, including both undifferentiated and differentiated cells. Therefore, the statement that the successful infection of a host requires terminally differentiated cells is false.

The gE-gI protein of HSV-1 is known to be a virally-encoded Fc-gamma receptor that is present in both the virus envelope and the cell membrane of infected cells. This protein plays a role in protecting the virus from clearance by the immune system. Antibody-dependent cell cytotoxicity (ADCC) is a mechanism by which immune cells, such as natural killer cells, recognize and kill virus-infected cells that are bound by antibodies. Since gE-gI is a receptor for antibodies, it is likely to affect ADCC, as it may interfere with the recognition and killing of infected cells by immune cells.

The homologue of IL-10 encoded by the Orf virus would mostly affect the T helper 1 response. IL-10 is a cytokine that plays a role in regulating the immune response. It is known to suppress the activity of T helper 1 cells, which are involved in cellular immunity and the production of pro-inflammatory cytokines. Therefore, the presence of the IL-10 homologue in the Orf virus would likely dampen the T helper 1 response, potentially allowing the virus to evade the immune system and establish infection.

The virulence mechanism described in the question is toxicity. The viral protein NSP4 produced by the rotavirus alters the permeability of intestinal epithelial cell tight junctions and inhibits the glucose-coupled Na+ transport of these cells. This leads to an increase in the osmotic gap and ultimately causes the watery diarrhea experienced by the child. This mechanism is considered toxic as it directly affects the normal functioning of the intestinal cells and disrupts their ability to absorb water and electrolytes properly.

Terminally differentiated cells, such as neurons, are permissive to viral infection. This means that these cells are susceptible to being infected by viruses. Unlike other cell types that may have defense mechanisms to prevent viral entry, terminally differentiated cells do not have these protective mechanisms, making them more vulnerable to viral infection. This is why viruses can successfully infect and replicate within neurons and other terminally differentiated cells.

The correct answer is "Modes of viral transmission seldom dictate the tissues that will be infected, but infected tissues often determine modes of transmission." This statement suggests that viral transmission does not have a strong influence on which tissues will be infected, but once a tissue is infected, it can determine how the virus is transmitted. This implies that the choice of tissues infected is not random, but the mode of transmission can vary depending on the infected tissue.

During viral infections, besides cell lysis, the most common modes of tissue damage are cell destruction by NK cells and cell destruction by CTLs. NK cells and CTLs are part of the immune system and play a crucial role in eliminating virus-infected cells. They recognize and kill these cells, leading to tissue damage. Mast cells, macrophages, and neutrophils are also involved in the immune response to viral infections but are not the primary cells responsible for cell destruction.