Genitourinary Infections

Chlamydia trachomatis

Most common STI worldwide
Obligate intracellular
Affects women more
Usually asymptomatic
Requires eukaryotic cell culture for growth
Diagnosed using molecular techniques

EB enters epithelial cell
Differentiates into RB
RB replicates, inclusion fusion
Either persists or differentiates into EB
Released via extrusion or lysis
Cycle repeats every ~48 hours

Describe the replication cycle of C. trachomatis.

MOMP
Pmps
Tarp
T3SS
Inc Proteins
Hsp60
CPAF
Plasmid-encoded (pgp3/pgp4)

What are the major virulence factors of C. trachomatis?

Porin, immune evasion

MOMP function

Adhesion, antigenic variation

Pmps function

Actin polymerization via T3SS

T3SS function

Prevent lysosomal fusion

Inc proteins function

Stress response, chronic inflammation

Hsp60 function

Degrades host proteins, inhibits apoptosis

CPAF function

Virulence, gene regulation

Plasmid-encoded (pgp3/pgp4) function

2nd most common STI
Gram-negative diplococcus
Aerobic
Affects genital, anal, ocular, nasopharyngeal mucosa
Requires iron (transferrin, lactoferrin, hemoglobin)

What are the defining characteristics of N. gonorrhoeae?

Pili
Por proteins
Opa proteins
RMP proteins
LOS
Capsule, Antigenic Variation

List the major virulence factors of N. gonorrhoeae.

Attachment, invasion, genetic exchange

Pili function

Prevent phagosome-lysosome fusion

Por proteins function

Colony adhesion, cell attachment

Opa proteins function

IgG interference

RMP proteins function

Triggers TNF-α, endotoxic effects

LOS function

Gp120
Gp41
Reverse transcriptase
Integrase
Protease
Gag polyprotein

What are the key structural proteins and enzymes in HIV?

Binds CD4 receptor

Gp120 function

Viral-host membrane fusion

Gp41 function

RNA to DNA

Reverse transcriptase function

Genome integration

Integrase function

Polyprotein cleavage

Protease function

Structural components

Gag polyprotein function

Attachment Gp120 to CD4
RNA Release
Reverse Transcription
Viral capsid disassembly
Integration into host genome
Latency or transcription
Protein synthesis
Viral assembly
Budding

Describe the stages of HIV replication.

Latent infection in memory cells
Escapes detection by antiretrovirals
Can reactivate upon Ag exposure or drug withdrawal

How does HIV evade the immune system?

L1
L2
E6
E7
E1/2
E4
E5

What are the key capsid and oncogenic proteins of HPV?

major capsid

L1 function

Minor capsid

L2 function

Binds p53

E6 function

Binds pRB

E7 function

Viral replication

E1/E2 function

Viral release

E4 function

Immune evasion

E5 function

High tropism for epithelial cells
Starts at basal layer → receptor-mediated endocytosis
Replication in nucleus (episomal)
Early gene expression → late gene expression
Assembly → virion release from upper layers

Describe HPV replication.

Detect unculturable organisms (e.g., Chlamydia)
Rapid identification
Differentiate related species
High sensitivity and specificity
Surveillance and epidemiology

What are the uses of molecular techniques in STI diagnostics?

Nontreponemal (VDRL, RPR): Screening, treatment monitoring
Treponemal (FTA-ABS, EIAs): Confirmatory, not for treatment monitoring

Compare Treponemal vs. Nontreponemal tests for Syphilis.

Entry inhibitors
Reverse transcriptase inhibitors
Integrase inhibitors (e.g., Dolutegravir)
Protease inhibitors
Maturation inhibitors

What are the targets of ART in HIV?

Tenofovir + Lamivudine + Dolutegravir

What is the first-line HIV treatment regimen in the Philippines?

Fast (<30 min), low-tech, no electricity
Easy to use, built-in controls
Examples: Lateral flow, ICT, microfluidic assays

What are the key features and examples of POCT?

Types 6 & 11
Types 16 & 18

What HPV types are associated with:
(a) Genital warts
(b) Cervical cancer?

Plasmid replication: Early stage in basal cells
Vegetative replication: In keratinocytes, high virion output

Define the two types of HPV replication.