Workshop 1 Flashcards
Q: What type of genome does Herpes Simplex Virus (HSV) have?
A: HSV has a double-stranded DNA (dsDNA) genome, enclosed in a nucleocapsid, surrounded by a tegument layer of viral proteins, and a lipid envelope with viral glycoproteins.
Q: How do HSV-1 and HSV-2 transmit between individuals?
A: HSV-1 and HSV-2 can transmit through direct contact (e.g., kissing, sexual intercourse) or indirect contact (e.g., sharing drinks). They can also be shed asymptomatically.
Touching someone’s arm—where there are no sores or mucous membranes—is highly unlikely to transmit the virus. HSV typically needs to enter through a break in the skin or mucous membranes (like the mouth or genitals) for transmission to occur. So casual contact like touching someone’s arm doesn’t pose a risk unless there is direct contact with infected areas.
Q: Describe the process of HSV replication in host cells.
A: HSV virions (viral particles) attach to host receptors, enter the cell via fusion or endocytosis, and transport their nucleocapsid to the nucleus. There, the viral genome is transcribed, viral proteins are produced, and new virions are assembled and released by exocytosis or cell lysis.
==> sometimes infected cell may lyse (burst), releasing a large number of new virions all at once. Lysis kills the host cell because it ruptures the cell membrane, and this is a common outcome for cells that are heavily infected. [viruses “prefer” to keep cells alive for as long as possible to produce more virions]
==> HSV replication eventually damages the host cell by depleting its resources, disrupting its normal functions, and triggering stress responses
Q: How does HSV establish latency in the body?
A: HSV initially replicates in epidermal cells, then enters sensory neurons, where it becomes latent in the nucleus of neurons in dorsal root or trigeminal ganglia. Reactivation occurs later, leading to recurrent lesions.
- primary infection, replicates immediately
2.After the virus replicates in the skin or mucosa, some of the newly made virions enter nearby sensory neurons (nerve cells).
HSV-1 usually travels to the trigeminal ganglion (near the face).
HSV-2 usually travels to the sacral ganglion (near the base of the spine).
Q: What are some immune responses triggered by HSV infection?
A: HSV infection is recognized by pattern recognition receptors (PRRs) in epithelial and immune cells
–> recognize PAMPs (Pathogen-Associated Molecular Patterns), which are molecules commonly found on pathogens like viruses, bacteria, and fungi but not on host cells.
=> For example, Toll-like receptors (TLRs) and cytosolic DNA receptors can detect HSV’s double-stranded DNA.
–> leading to the production of type I interferon, proinflammatory cytokines, and the recruitment of immune cells like NK cells and T cells to control the infection.
Q: How do NK cells contribute to controlling HSV infections?
A: NK cells detect and kill HSV-infected cells that lack MHC-I expression. They produce interferon gamma and cytolytic granules, which are crucial for the control of HSV, especially in recurrent or severe infections.
• Many viruses, including HSV, can interfere with the expression of MHC Class I on the surface of infected cells. This is a strategy viruses use to evade detection by cytotoxic T cells (CD8+ T cells), which rely on MHC Class I to recognize and destroy infected cells. • However, NK cells are designed to detect this absence of MHC Class I. Under normal conditions, healthy cells express MHC Class I, which sends an “inhibitory signal” to NK cells, preventing them from attacking. • When a cell loses MHC Class I expression due to viral infection (or cancer), this inhibitory signal is lost. As a result, NK cells are activated and can kill the infected cell.
Q: why is it harmful and What complications can arise from HSV infections?
- Cell damage and death: When HSV replicates in skin or mucosal cells, it causes cell death, which leads to blisters (fluid-filled lesions full of viral particles). These blisters are painful, as the virus destroys tissue. The immune response to this damage can cause inflammation, swelling, and discomfort.
- Inflammation and immune response:
A: Complications include neurological issues like encephalitis or meningitis, vertical transmission leading to neonatal infections, and increased risk of HIV acquisition in individuals with genital lesions.
Q: How is HSV treated and controlled?
A: HSV infections are treated with antiviral drugs like Acyclovir, which inhibits viral replication. To control transmission, sexual abstinence during lesions and condom use are recommended, and caesarean delivery is advised to prevent neonatal exposure.
Q: How does the male genitourinary system’s microbiota compare to that of the female system?
A: The male genitourinary microbiota is primarily confined to the distal urethra and resembles skin microbiota like Staphylococcus and Micrococcus. In contrast, the female system is more dynamic, changing with factors like age and the menstrual cycle.
Q: What role does T. vaginalis’ cysteine proteinase play in infection?
A: T. vaginalis secretes cysteine proteinase CP65, which is highly functional at pH 5.5, degrading host proteins like collagen and fibronectin in vaginal cells, causing tissue damage and promoting infection.
Q: How does Neisseria gonorrhoeae evade the host immune system?
A: N. gonorrhoeae uses Type IV pili for adherence = to epithelial cells, attachment to colonist and infect body
immune evasion via antigenic variation,
The pili undergo frequent changes in their structure (antigenic variation), allowing the bacteria to evade the host’s immune system by constantly altering their appearance.
and produces PorB protein to inactivate complement pathways.
porin protein that forms channels in the bacterial outer membrane, allowing the transport of ions and nutrients into the cell. This is essential for bacterial survival.
• Immune Modulation: PorB can interfere with host immune responses by preventing the fusion of phagosomes and lysosomes in immune cells, helping N. gonorrhoeae survive inside these cells.
• Host Cell Interaction: PorB also helps in the interaction with host cells, facilitating the bacteria’s entry into the cells and contributing to immune evasion.
It also secretes IgA protease to degrade IgA antibodies, aiding tissue invasion, weakening the host’s immune defense.
Q: How does Chlamydia trachomatis invade host cells?
A: C. trachomatis uses a Type III secretion system to inject the TARP protein into host cells, rearrangement of host cell actin cytoskeleton, remodeling them to allow bacterial survival and replication. CPAF (degrade host cell proteins, including transcription factors for initiating immune responses] and Pgp3 proteins also help the bacteria evade host antimicrobial peptides.
Q: What is the role of microbial virulence genes in HSV-1?
A: The thymidine kinase (TK) gene (UL23) is essential for HSV-1 reactivation from latency, while the US3 gene reduces type I interferon production. The ICP34.5 gene is critical for neurovirulence and inhibits autophagy in host neurons.
Normally, cells respond to viral infections by shutting down protein synthesis through a pathway involving PKR (Protein Kinase R), which phosphorylates a protein called eIF2α. This phosphorylation halts protein production, which limits viral replication.
• ICP34.5 reverses this phosphorylation by interacting with cellular proteins to recruit a phosphatase (PP1), which dephosphorylates eIF2α, allowing protein synthesis to continue. This action ensures that HSV can continue replicating inside the host cell.
Q: What is the role of Lactobacillus in the female genitourinary system?
A: Lactobacillus produces lactic acid, maintaining a low pH (4-5) environment in the vagina, inhibiting pathogen growth. It also produces hydrogen peroxide and bacteriocins, which prevent pathogen colonization by competing for binding sites and nutrients.
Q: How does the lower female genital tract differ from the upper tract in terms of epithelial cell structure and infection defense?
A: The lower female genital tract (ectocervix and vagina) has stratified non-keratinized squamous epithelial cells, which provide a thicker barrier against infection but have a larger surface area for potential pathogen interactions.
Q: What is the primary defense mechanism of the upper female genital tract?
A: The upper female genital tract (fallopian tubes, uterus, and endocervix) is lined with a single layer of columnar epithelial cells joined by tight junctions, limiting microbial entry. The mucus layer also contains antimicrobial peptides, defensins, and antibodies.
interferon y (gamma)/ type 1 = gamma + alpha
Who produces it? Mainly produced by Natural Killer (NK) cells and T cells (specifically, CD4 and CD8 T cells).
What does it do?
1. Activates immune cells: IFN-γ enhances the activity of macrophages and other immune cells, making them more effective at killing infected cells and clearing infections.
2. Promotes an antiviral state: It increases the production of MHC molecules (Major Histocompatibility Complex) on the surface of cells. This helps infected cells present viral antigens more efficiently to T cells, allowing T cells to recognize and kill them.
3. Limits viral replication: IFN-γ creates an environment that is hostile to viruses by interfering with their ability to replicate within host cells.
Cytolytic Granules:
Who produces them? These are produced by Natural Killer (NK) cells and Cytotoxic T cells (CD8 T cells).
What do they do?
1. Directly kill infected cells: Cytolytic granules contain proteins like perforin and granzymes.
–> Perforin: This protein forms pores in the membrane of an infected cell. the main purpose of these pores is to allow other molecules, like granzymes, to enter the cell.
–> Granzymes: These are enzymes that enter the infected cell through the perforin pores and trigger apoptosis (programmed cell death). This ensures the infected cell is destroyed before it can produce more viral particles.
interferon alpha (IFN-α), and interferon beta (IFN-β)
Both IFN-α and IFN-β belong to the Type I interferon family, primary role is to help cells establish an antiviral state early during viral infections.
==> When they are produced: Type I interferons are typically produced in response to the early detection of a viral infection. Pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), recognize viral components like viral RNA or DNA and trigger the production of IFN-α and IFN-β.
What they do:
Antiviral defense: They signal nearby cells to adopt an “antiviral state,” making it harder for the virus to replicate. This can prevent the virus from spreading to neighboring cells.
Boost immune activity: They stimulate the activation of other immune cells, like natural killer (NK) cells and macrophages.
Upregulate MHC expression: They increase the expression of MHC class I molecules on infected cells, making it easier for cytotoxic T cells to recognize and kill those cells.
the differences between interferon gamma (IFN-γ), interferon alpha (IFN-α), and interferon beta (IFN-β)
Both IFN-α and IFN-β belong to the Type I interferon family, and they are very similar in function. Their primary role is to help cells establish an antiviral state early during viral infections.
==> When they are produced: Type I interferons are typically produced in response to the early detection of a viral infection. Pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), recognize viral components like viral RNA or DNA and trigger the production of IFN-α and IFN-β.
Type 2/ Gamma:
IFN-γ is produced later in the immune response, particularly during adaptive immunity when the body has recognized a pathogen and is mounting a more specific response.
T. vaginalis who what how
T. vaginalis refers to Trichomonas vaginalis, a protozoan parasite (not a virus or bacteria).
It is a protist parasite, a type of single-celled eukaryotic microorganism
It is primarily transmitted through sexual contact.
Trichomoniasis, which affects both men and women, though women tend to have more noticeable symptoms.
Neisseria gonorrhoeae who what how
a bacterium that causes the sexually transmitted infection gonorrhea.
Gram-negative diplococcus (a type of round-shaped bacterium that typically forms in pairs).
Gonorrhea, a sexually transmitted infection (STI), which primarily affects the mucous membranes of the reproductive tract, but can also infect the throat, eyes, and rectum.
Chlamydia trachomatis who what how
Chlamydia trachomatis is a bacterium that causes chlamydia, another common sexually transmitted infection (STI). It is an obligate intracellular pathogen, meaning it can only replicate inside human cells.
Gram-negative bacterium, although its structure is somewhat atypical due to its unique developmental cycle.
\Chlamydia, which affects the reproductive tract. It can also cause infections in the eyes (trachoma), respiratory system, and rectum.
Gram-Positive Bacteria
Thick peptidoglycan layer: The cell wall of Gram-positive bacteria consists of a thick layer of peptidoglycan, which is a mesh-like structure made of sugars and amino acids. This thick layer helps the bacteria retain the crystal violet dye, giving them a purple appearance under a microscope after Gram staining.
No outer membrane: Gram-positive bacteria lack an outer membrane, which is present in Gram-negative bacteria.
Stain result: Purple (because the thick peptidoglycan layer traps the crystal violet dye).
Examples:
Staphylococcus aureus (causes skin infections)
Streptococcus pyogenes (causes strep throat)
Lactobacillus (beneficial bacteria in the gut and vagina)
Susceptibility to antibiotics: Gram-positive bacteria are often more susceptible to antibiotics like penicillin, which target the peptidoglycan in the cell wall, disrupting its structure.
