1. HSV – Virology & Microbiology (What is this virus?)
1.1 Basic classification
- Family: Herpesviridae
- Type: Enveloped, double-stranded DNA virus
- Subfamily: Alphaherpesviridae (rapid replication, latency in sensory ganglia)
- Serotypes:
- HSV-1 – classically orolabial, but increasingly genital
- HSV-2 – classically genital (most recurrent genital herpes in adults)
Key memory:
Herpes = enveloped dsDNA + lifelong latent in sensory ganglia
1.1 Basic classification — Active Recall (Fill in the Blanks)
- Family: _____________
- Type: _____________, _____________-stranded _____________ virus
- Subfamily: _____________ (rapid replication, latency in _____________ _____________)
Serotypes
- HSV-1 – classically _____________, but increasingly _____________
- HSV-2 – classically _____________ (most _____________ genital herpes in _____________)
Key Memory Line
- Herpes = _____________ _____________ + lifelong _____________ in _____________ _____________
1.2 Structure
- Core: linear dsDNA genome
- Capsid: icosahedral
- Tegument: protein layer around capsid (contains viral proteins that help early replication)
- Envelope: lipid bilayer derived from host, with multiple glycoproteins (gB, gC, gD, gH, etc.) → needed for binding & entry.
Clinical relevance:
- Envelope → sensitive to drying, detergents, disinfectants
- Close contact required (sexual, perinatal, mucosal).
1.2 Structure — Active Recall (Fill in the Blanks)
- Core: linear __________ genome
- Capsid: __________ symmetry
- Tegument: __________ layer around capsid containing viral __________ that help __________ replication
- Envelope: __________ bilayer derived from __________, with multiple __________ (gB, gC, gD, gH, etc.) required for __________ and __________
Clinical Relevance — Active Recall
- Presence of envelope → virus is __________ to __________, __________, and __________
- Therefore, transmission requires __________ __________
- Common modes: __________, __________, and __________ contact
1.3 Replication cycle (why latency/recurrent?)
- Attachment to host cell
- Viral glycoproteins bind to host receptors (e.g. heparan sulfate, nectin-1).
- Fusion & entry
- Envelope fuses with cell membrane → capsid + tegument enter cytoplasm.
- Transport to nucleus
- Capsid goes to nuclear pore → viral DNA enters nucleus.
- Gene expression (immediate-early → early → late genes)
- Immediate-early: regulatory proteins
- Early: DNA polymerase etc.
- Late: structural proteins (capsid, glycoproteins)
- DNA replication – rolling circle mechanism.
- Assembly in nucleus → nucleocapsids.
- Envelopment via host membranes → virions released by exocytosis or cell lysis.
Active Recall — Fill in the Blanks
1. Attachment to host cell
- Viral _____________ bind to host receptors such as _____________ _____________ and _____________-___________.
2. Fusion & entry
- Viral _____________ fuses with the _____________ _____________ → _____________ + _____________ enter the _____________.
3. Transport to nucleus
- _____________ travels to the _____________ _____________ → viral _____________ enters the _____________.
4. Gene expression sequence
- Occurs in the order: __ → _____________ → _____________ genes.
Subtypes
- Immediate-early genes code for _____________ _____________.
- Early genes code for _____________ _____________ (e.g., _____________ _____________).
- Late genes code for _____________ _____________ such as _____________ and _____________.
5. DNA replication
- Viral DNA replicates via the _____________ _____________ mechanism.
6. Assembly
- Assembly occurs in the _____________ forming _____________.
7. Envelopment & release
- Envelopment occurs via _____________ _____________ → virions released by _____________ or _____________ _____________.
1.4 Latency & reactivation (very examworthy)
- After primary infection, virus travels retrograde in sensory nerves to the sensory ganglia:
- Genital HSV → sacral dorsal root ganglia (S2–S4)
- Oral HSV → trigeminal ganglion
- In latency:
- Viral DNA persists as episome in nucleus
- Only latency-associated transcripts (LATs) expressed – no full viral replication.
- Reactivation triggers:
- Stress, fever, sunlight, menstruation, immunosuppression, pregnancy.
- Reactivation → virus travels anterograde down nerve → recurrent lesions on skin/mucosa.
Key exam line:
HSV establishes lifelong latency in sensory ganglia with periodic reactivation causing recurrent lesions.
1.4 Latency & Reactivation — Active Recall (Fill in the Blanks)
After Primary Infection
- After primary infection, HSV travels _____________ in _____________ nerves to the _____________ _____________.
- Genital HSV → _____________ _____________ _____________ _____________ (–)
- Oral HSV → _____________ _____________
During Latency
- Viral DNA persists in the nucleus as an _____________.
- Only _____________ (_________) are expressed.
- During latency, there is no full viral _____________.
Reactivation Triggers
- Common reactivation triggers include:
Reactivation & Recurrence
- During reactivation, virus travels _____________ down the nerve.
- This results in _____________ _____________ on the _____________ or _____________.
Key Exam Line (Fill in the Blanks)
- HSV establishes lifelong _____________ in _____________ _____________ with periodic _____________ causing _____________ _____________.
1.5 Transmission (focus on pregnancy)
- Sexual contact – genital-genital, oral-genital.
- Vertical transmission:
- Mostly intrapartum (during delivery) from contact with infected genital secretions.
- Rarely in utero (transplacental) or postnatally (direct contact, kissing, breast lesions).
Transmission risk is highest when:
- Mother has primary HSV infection near term, especially if she is shedding virus and has no antibodies yet.
1.5 Transmission (Focus on Pregnancy) — Active Recall
Modes of Transmission
- Sexual contact includes:
- –
- –
Vertical Transmission
- Vertical transmission occurs most commonly _____________ (during _____________).
- The main mechanism is contact with infected _____________ _____________.
- Vertical transmission may rarely occur:
- _____________ (_____________)
- _____________ (direct _____________, _____________, _____________ _____________)
Highest Risk Scenario
- Transmission risk is highest when the mother has _____________ HSV infection _____________ _____________.
- Risk is especially high if she is _____________ _____________ and has _____________ _____________ yet.
1.6 Immune response (why primary infection is dangerous)
- Innate:
- Interferons, NK cells.
- Adaptive:
- Humoral: neutralizing antibodies → reduce severity of subsequent infections.
- Cell-mediated immunity is critical (CD8+ T cells).
- In primary infection in pregnancy, mother is seronegative, no pre-existing antibodies → higher viraemia, higher risk to fetus/neonate.
1.6 Immune Response (Why Primary Infection Is Dangerous)
Active Recall — Fill in the Blanks
Innate Immunity
- Key innate immune components include _____________ and _____________ .
Adaptive Immunity
- Humoral immunity involves _____________ _____________ which reduce the _____________ of subsequent infections.
- Cell-mediated immunity is _____________ and is mediated mainly by _____________+ __cells.
Primary Infection in Pregnancy
- In primary HSV infection during pregnancy, the mother is _____________.
- There are no pre-existing _____________.
- This leads to higher _____________ and increased risk to the _____________
2. Clinical patterns of HSV relevant to pregnancy
2.1 Primary genital HSV infection
- First episode in seronegative woman (no prior HSV-1/2 antibodies).
- Features:
- Painful grouped vesicles → ulcers on vulva, vagina, cervix, perineum.
- Marked pain, dysuria, tender inguinal lymphadenopathy, fever, malaise.
- Lesions last longer (2–3 weeks) than recurrent episodes.
- Obstetric importance:
- If occurs in 1st trimester → small risk miscarriage / congenital HSV (rare).
- If occurs in 3rd trimester, especially near delivery → high risk of neonatal HSV if vaginal birth.
2.1 Primary Genital HSV Infection — Active Recall
Definition
- Primary genital HSV infection is the first episode in a _____________ woman with no prior __________- / _____________.
Clinical Features
- Painful _____________ _____________ progress to _____________ on the _____________, _____________, _____________, and _____________.
- Associated symptoms include:
- Marked _____________
- Tender _____________ _____________
- Lesions persist for __– _____________, which is _____________ than recurrent episodes.
Obstetric Importance
- Infection in the _____________ trimester carries a small risk of _____________ or _____________ HSV (_____________).
- Infection in the _____________ trimester, especially _____________ _____________, carries a _____________ risk of _____________ HSV if _____________ birth occurs.
2.2 Non-primary first episode
- Genital infection with one HSV type in a woman already immune to the other type
- Less severe than true primary, some cross-protection.
(e.g. prior HSV-1 orolabial → now genital HSV-2).
2.2 Non-Primary First Episode — Active Recall
- A non-primary first episode is a _____________ infection with one _____________ type in a woman already _____________ to the _____________ type.
- Example: prior _____________ _____________ infection → current _____________ _____________ infection.
- Compared to a true primary infection, this episode is _____________ _____________.
- This is because there is partial between HSV types.
2.3 Recurrent genital HSV
- Reactivation from sacral ganglia.
- Mild prodromal tingling, burning → fewer lesions, faster healing (5–7 days).
- Systemic symptoms usually minimal.
- In pregnancy: much lower risk of neonatal infection compared with primary, because maternal antibodies present.
2.3 Recurrent Genital HSV — Active Recall
- Recurrent genital HSV results from _____________ from the _____________ _____________.
- Patients often experience mild _____________ symptoms such as _____________ and _____________ before lesions appear.
- Recurrent episodes are characterized by _____________ lesions and _____________ healing.
- Lesions typically heal within __– ____ _________.
- _____________ symptoms are usually _____________ .
Pregnancy Relevance
- In pregnancy, recurrent genital HSV carries a _____________ _____________ of _____________ infection compared with primary infection.
- This reduced risk is because _____________ _____________ are _____________.
2.4 HSV in the fetus/neonate (for viva/short notes)
- In utero (congenital) – rare:
- Microcephaly, chorioretinitis, skin scarring, IUGR, hydrocephalus.
- Neonatal HSV – acquired around delivery:
- Localized skin/eye/mouth disease.
- CNS disease – encephalitis.
- Disseminated disease – multi-organ failure, high mortality.
Risk of neonatal HSV:
- Primary maternal infection near delivery: up to ~30–50%
- Recurrent infection with lesions at delivery: ~1–3%
- Asymptomatic shedding: smaller but real risk.
(Exact numbers vary by source, but concept = primary near term = highest risk.)
2.4 HSV in the Fetus / Neonate — Active Recall
In Utero (Congenital) Infection
- In-utero (congenital) HSV infection is _____________.
- Congenital HSV may present with:
Neonatal HSV (Around Delivery)
- Neonatal HSV is usually acquired _____________ _____________.
- The three major clinical forms are:
- _____________ _____________ / _____________ / _____________ disease
- _____________ disease – _____________
- _____________ disease – failure with _____________ mortality
Risk of Neonatal HSV
- Risk with _____________ maternal infection _____________ _____________ is approximately _____________–___________%.
- Risk with _____________ infection and _____________ at delivery is approximately _____________–___________%.
- _____________ viral _____________ carries a _____________ but _____________ risk.
3. Diagnosis (mother during pregnancy)
- Clinical: characteristic painful vesicles/ulcers.
- Lab tests:
- PCR from lesion swab – most sensitive & specific (type-specific, HSV-1 vs HSV-2).
- Viral culture (less used now).
- Type-specific HSV serology (IgG) to distinguish primary vs recurrent:
- Primary = no prior antibodies, new seroconversion.
- In pregnancy, diagnosis often clinical + PCR if needed.
Diagnosis (mother during pregnancy) – Active Recall
Clinical
- Diagnosis is often __________ based on __________ painful __________ / __________.
Laboratory tests
- Most sensitive and specific test: __________ from __________ swab
- Can differentiate __________ vs __________.
- Older method now less used: __________ __________.
- To distinguish primary vs recurrent infection:
- Type-specific HSV __________ (__________)
- Primary infection = no prior __________, with new __________.
In pregnancy
- Diagnosis is usually __________ + __________ (if confirmation is needed).
4. Antiviral drugs (Mechanism + names)
- Acyclovir (and its prodrug valacyclovir): mainstay.
- They are guanosine analogues:
- Activated by viral thymidine kinase → acyclovir triphosphate.
- Inhibits viral DNA polymerase → chain termination.
- Safe and widely used in pregnancy and breastfeeding (especially acyclovir).
4. Antiviral drugs (Mechanism + names) – Active Recall
Main drugs
- First-line drug for HSV: __________
- Prodrug with better oral bioavailability: __________
Drug class
- These drugs are __________ analogues.
Activation
- Initial phosphorylation is done by __________ __________ __________.
- Active form is __________ __________ .
Mechanism of action
- Inhibits __________ __________ __________.
- Results in __________ __________ of viral DNA.
Use in pregnancy
- These drugs are considered __________ and used in __________ and __________.
5. HSV in Pregnancy – Management Strategy
Think in 3 big questions:
- Is this primary or recurrent genital herpes?
- What gestation? Early vs near term.
- At delivery, are there active lesions / prodromal symptoms?
5.1 General principles
- Do not terminate pregnancy solely for genital herpes.
- Aim to:
- Treat maternal symptoms.
- Reduce viral shedding.
- Prevent neonatal HSV – especially at delivery.
5. HSV in Pregnancy – Management Strategy (Active Recall)
Three key questions
- Is the infection __________ or __________ genital herpes?
- What is the __________ age? __________ vs __________ pregnancy.
- At delivery, are there __________ __________ or __________ __________?
5.1 General principles
- Pregnancy should __________ be __________ solely due to genital herpes.
- Management aims to:
- __________ maternal symptoms.
- __________ viral shedding.
- __________ __________ HSV, especially at __________.
5.2 Management of primary genital HSV in pregnancy
A. During pregnancy (not at labour)
- Confirm clinically ± PCR.
- Oral acyclovir:
- Typical regimen: Acyclovir 400 mg TDS (three times daily) for 5–10 days
- Analgesia, local care (saline baths, topical anesthetic gel).
- Counsel:
- Avoid sexual contact (especially oral-genital) during active lesions.
- Use condoms thereafter (reduces but does not fully prevent transmission).
(Exact dose/duration can vary by guideline; know “acyclovir for 5–10 days”).
If primary infection occurs in 1st or 2nd trimester:
- Treat with acyclovir as above.
- Reassure: congenital infection is rare.
- Document HSV status in notes.
- Plan suppressive therapy from 36 weeks onwards (see below).
If primary infection occurs in 3rd trimester, especially within 6 weeks of delivery:
- High risk of neonatal infection if vaginal birth.
- Start oral acyclovir immediately.
- Plan elective caesarean section at onset of labour / rupture of membranes IF active lesions or infection within last ~6 weeks.
- Also start suppressive therapy from 36 weeks (see below) to reduce viral shedding and necessity for emergency CS.
5.2 Management of primary genital HSV in pregnancy – Active Recall
A. During pregnancy (not at labour)
- Diagnosis is __________ ± __________.
- First-line antiviral:
- Oral __________
- Typical regimen: __________ mg __________ (__________ times daily) for – days
- Supportive care:
- __________
- __________ care (e.g. saline baths, topical __________ gel)
Counselling
- Avoid __________ contact during active lesions (especially –).
- Use __________ thereafter:
- Reduces transmission but does __________ fully __________ it.
If primary infection occurs in 1st or 2nd trimester
- Treat with __________ as above.
- Reassure: congenital infection is __________.
- __________ HSV status clearly in antenatal notes.
- Plan __________ therapy from __________ weeks onwards.
If primary infection occurs in 3rd trimester (especially within __________ weeks of delivery)
- Risk of __________ HSV infection is __________ if vaginal delivery.
- Start oral __________ __________.
- Plan __________ caesarean section at:
- Onset of __________ or
- __________ of membranes
- IF __________ lesions are present or infection occurred within last __________ weeks.
- Also commence __________ therapy from __________ weeks to:
- Reduce __________ shedding
- Reduce need for __________ CS.
5.3 Management of recurrent genital HSV in pregnancy
- Recurrent episodes:
- Treat with short course oral acyclovir (e.g. 400 mg TDS for 5 days).
- Routine antenatal care continues.
Suppressive therapy (very exam-high-yield)
- For women with:
- Frequent recurrences, OR
- Primary infection earlier in pregnancy, OR
- Known genital HSV to reduce lesions at delivery.
From 36 weeks until delivery:
- Acyclovir 400 mg orally TDS
(or Valacyclovir 500 mg BD where available).
Benefits:
- Reduces clinical recurrences.
- Reduces asymptomatic shedding.
- Reduces need for caesarean for HSV.
5.3 Management of recurrent genital HSV in pregnancy – Active Recall
Recurrent episodes
- Managed with __________ course oral __________.
- Example regimen: __________ mg __________ for __________ days.
- __________ antenatal care continues.
Suppressive therapy (exam-high-yield)
Indications (any ONE):
- __________ recurrences
- __________ infection earlier in pregnancy
- Known __________ HSV to reduce lesions at delivery
Timing
- Start from __________ weeks until __________.
Drug & dose
- __________ __________ mg orally __________
- Alternative (where available): __________ __________ mg __________
Benefits
- Reduces __________ recurrences
- Reduces __________ viral __________
- Reduces need for __________ section for HSV
5.4 Management at time of delivery
A. Primary genital HSV near term or at labour
- Active primary lesions or prodromes (pain, burning) at onset of labour:
- Recommend caesarean section to reduce neonatal HSV.
- Ideally done within 4–6 hours of membrane rupture for maximal benefit, but still beneficial later.
- if > 6 hrs has passed give iv Acyclovir to baby for 10 days
B. Recurrent genital HSV at labour
- If recurrent lesions or prodrome present at onset of labour:
- Many guidelines recommend caesarean section, especially if first episode or frequent recurrences.
Recurrent lesions at labour → offer caesarean section to reduce neonatal risk.
- If no active lesions and no prodromes at delivery:
- Vaginal delivery is safe, even if maternal history of HSV.
- Suppressive acyclovir from 36 weeks helps.
C. Spontaneous rupture of membranes (SROM)
- Primary HSV with active lesions + SROM:
- Proceed to caesarean section as soon as possible; risk increases with duration of ruptured membranes.
- Recurrent HSV with lesions + SROM:
- Usually still offer CS, but risk somewhat lower.
5.4 Management at time of delivery – Active Recall
A. Primary genital HSV near term or at labour
- If __________ primary __________ or __________ (__________, __________) are present at __________ of __________:
- __________ caesarean section to reduce __________ HSV.
- Optimal timing:
- Ideally within – hours of __________ rupture.
- Still __________ even if done later.
B. Recurrent genital HSV at labour
- If __________ lesions or __________ present at __________ of __________:
- Most guidelines recommend __________ __________, especially if:
- __________ episode, or
- __________ recurrences.
- Exam-standard rule:
- Recurrent lesions at labour → __________ __________ to reduce __________ risk.
- If __________ active lesions AND __________ prodromes at delivery:
- __________ delivery is __________.
- Applies even with __________ history of HSV.
- __________ acyclovir from __________ weeks reduces risk.
C. Spontaneous rupture of membranes (SROM)
- __________ HSV with __________ lesions + __________:
- Proceed to __________ section as __________ as possible.
- Neonatal risk __________ with __________ of ruptured membranes.
- __________ HSV with __________ lesions + __________:
- Usually still __________ CS.
- Risk is __________ than with primary infection.
5.5 Postnatal management & breastfeeding
- Breastfeeding:
- HSV is not transmitted via breast milk.
- Breastfeeding is allowed if:
- No herpetic lesions on the breast.
- Mother practices hand hygiene.
- If lesions on breast → avoid feeding from that side until fully healed.
- Contact precautions:
- No kissing baby if orolabial lesions present.
- Handwashing after touching lesions.
- HSV is not transmitted via __________ __________.
- Breastfeeding is __________ if:
- No __________ __________ on the __________.
- Mother practices __________ __________.
- If __________ on the breast → avoid feeding from that __________ until fully __________.
- No __________ baby if __________ lesions are present.
- __________ after touching __________.
5.5 Postnatal management & breastfeeding – Active Recall (Blanks)
Breastfeeding:
Contact precautions:
6. Neonatal HSV – what to mention in an answer
If baby is born to mother with active genital HSV at delivery (especially primary):
- Assess neonate:
- Examine for lesions.
- Swabs (mouth, nasopharynx, conjunctiva, rectum) for HSV PCR.
- Blood tests, ± CSF if symptomatic.
- Empirical IV acyclovir if:
- Maternal primary HSV near delivery or
- Neonate symptomatic (lethargy, fever, seizures, respiratory distress, vesicles).
Typical neonatal regimen (conceptual, do not need exact doses in OBGYN exam):
- IV acyclovir for 14–21 days depending on disease type (local vs CNS vs disseminated).
Neonatal HSV – Active Recall (Fill in the Blanks)
If baby is born to mother with active __________ HSV at delivery (especially __________):
Assess neonate:
- Examine for __________.
- Swabs (__________, __________, __________, __________) for HSV __________.
- __________ tests, ± __________ if __________.
Empirical IV __________ if:
- Maternal __________ HSV near delivery or
- Neonate __________ (__________, __________, __________, __________, __________).
Typical neonatal regimen
(conceptual – exact doses not required in OBGYN exam):
- IV __________ for – days depending on disease type (__________ vs __________ vs __________).
7. HSV & pregnancy counselling points (for OSCE / viva)
- Explain:
- HSV is common; many adults infected.
- Once infected, virus stays in body and can recur.
- In pregnancy:
- High risk if first infection in late pregnancy.
- Lower risk with recurrent HSV because woman has antibodies.
- We use antiviral tablets (acyclovir) to:
- Make symptoms better.
- Reduce chances of passing virus to baby.
- We may recommend caesarean if infection is new or there are lesions at birth.
- Baby will be monitored, and if high risk, may need IV acyclovir.
8. “20% that gives 80% marks” – Exam-style condensation
If you’re short on time, this is what you MUST remember:
- Virus & latency
- HSV-1, HSV-2; enveloped dsDNA; Herpesviridae.
- Establishes lifelong latency in sensory ganglia with periodic reactivation.
- Transmission & pregnancy risk
- Transmission by sexual contact and perinatally during vaginal delivery.
- Highest risk of neonatal infection when primary maternal genital HSV occurs near term (mother seronegative, high shedding).
- Primary vs recurrent
- Primary: severe, systemic symptoms, longer duration, no antibodies, high neonatal risk if close to delivery.
- Recurrent: milder, shorter, antibodies reduce fetal/neonatal risk.
- Antiviral of choice
- Acyclovir – safe in pregnancy & breastfeeding.
- Treatment: e.g. 400 mg TDS for 5–10 days for acute episodes.
- Suppressive therapy from 36 weeks: acyclovir 400 mg TDS until delivery to reduce recurrences and viral shedding.
- Mode of delivery
- Primary HSV with active lesions or first-episode near term → caesarean section recommended to prevent neonatal HSV (especially if lesions or prodrome at labour).
- Recurrent HSV with no lesions / prodrome at labour → vaginal delivery is acceptable (especially if on suppressive therapy).
- Recurrent HSV with active lesions or prodrome at labour → usually offer caesarean.
- Neonate
- Risk: skin/eye/mouth disease, CNS disease, or disseminated infection.
- If high risk → investigate and give IV acyclovir early.
Herpetic whitlow = lesions on fingers from autoinnoculations
Eczema herpeticum = localized (on the eczema), Monomorphic lesions, pain full
TZANCK CELLS = inclusion bodies = Cowdry
complications
Erythema multiforme
steven Johnson syndrome
Sacral radiculopathy
Perfect — I’ll condense everything you listed into exam-safe, zero-omission master tables, arranged so you can revise fast, answer vivas, and convert to XMind easily.
No fluff, no missing links.
🦠 HSV — COMPLETE HIGH-YIELD TABLE SET (Zero Omission)
TABLE 1 — HSV VIROLOGY & STRUCTURE (FOUNDATION TABLE)
Aspect | Details |
Virus family | Herpesviridae |
Subfamily | Alphaherpesvirinae |
Genome | Double-stranded DNA (linear) |
Envelope | Present (lipid bilayer from host) |
Capsid | Icosahedral |
Tegument | Protein layer between capsid & envelope |
Glycoproteins | gB, gC, gD, gH (attachment & fusion) |
Replication speed | Rapid |
Site of replication | Nucleus |
DNA replication | Rolling circle mechanism |
Latency site | Sensory ganglia |
Environmental stability | Fragile (envelope sensitive) |
📌 Exam hook: Enveloped dsDNA virus → nuclear replication → lifelong latency
TABLE 2 — HSV-1 vs HSV-2 (SEROTYPE COMPARISON)
Feature | HSV-1 | HSV-2 |
Classical site | Orolabial | Genital |
Current trend | Increasing genital infections | Still main cause of recurrent genital HSV |
Latency ganglion | Trigeminal | Sacral (S2–S4) |
Neonatal HSV risk | Possible | Higher |
Recurrence frequency | Less frequent genital recurrence | More frequent recurrence |
TABLE 3 — HSV REPLICATION CYCLE (STEPWISE EXAM TABLE)
Step | Key Events |
Attachment | Glycoproteins bind heparan sulfate, nectin-1 |
Entry | Envelope fuses with cell membrane |
Transport | Capsid → nuclear pore |
Gene expression | Immediate-early → Early → Late |
Early genes | DNA polymerase, thymidine kinase |
Late genes | Capsid proteins, envelope glycoproteins |
DNA replication | Rolling circle |
Assembly | Nucleus |
Release | Exocytosis or cell lysis |
TABLE 4 — LATENCY & REACTIVATION (VERY EXAM-WORTHY)
Aspect | Details |
Nerve transport to ganglion | Retrograde axonal transport |
Genital HSV latency site | Sacral dorsal root ganglia (S2–S4) |
Oral HSV latency site | Trigeminal ganglion |
Latent genome form | Episome |
Genes expressed | Latency-associated transcripts (LATs) |
Full replication in latency | Absent |
Reactivation transport | Anterograde |
Reactivation triggers | Stress, fever, sunlight, menstruation, pregnancy, immunosuppression |
📌 Key line: HSV establishes lifelong latency with periodic reactivation.
TABLE 5 — TRANSMISSION (WITH PREGNANCY FOCUS)
Mode | Details |
Sexual | Genital–genital, oral–genital |
Vertical (main) | Intrapartum during delivery |
Mechanism | Contact with infected genital secretions |
In utero | Rare (transplacental) |
Postnatal | Kissing, skin contact, breast lesions |
Highest neonatal risk | Primary maternal infection near term |
Why high risk | No maternal antibodies + high viral shedding |
TABLE 6 — IMMUNE RESPONSE & PREGNANCY RISK
Component | Role |
Innate immunity | Interferons, NK cells |
Humoral immunity | Neutralizing antibodies |
Cell-mediated immunity | CD8⁺ T cells (CRITICAL) |
Primary infection in pregnancy | Mother seronegative |
Consequence | Higher viraemia |
Neonatal risk | High |
TABLE 7 — CLINICAL TYPES OF GENITAL HSV (PREGNANCY-RELEVANT)
Type | Features | Neonatal Risk |
Primary | Severe, systemic, long duration | Highest |
Non-primary first episode | Partial immunity, milder | Moderate |
Recurrent | Mild, short, prodrome | Low |
TABLE 8 — PRIMARY GENITAL HSV (DETAIL TABLE)
Aspect | Details |
Immune status | Seronegative |
Lesions | Painful vesicles → ulcers |
Sites | Vulva, vagina, cervix, perineum |
Systemic features | Fever, malaise, dysuria, lymphadenopathy |
Duration | 2–3 weeks |
1st trimester risk | Rare miscarriage / congenital HSV |
Near term risk | High neonatal HSV risk |
TABLE 9 — RECURRENT GENITAL HSV
Feature | Details |
Source | Reactivation from sacral ganglia |
Prodrome | Tingling, burning |
Lesions | Fewer |
Healing time | 5–7 days |
Systemic symptoms | Minimal |
Pregnancy risk | Low (antibodies present) |
TABLE 10 — FETAL & NEONATAL HSV
Type | Key Features |
Congenital (in utero) | Rare |
Congenital features | Microcephaly, hydrocephalus, chorioretinitis, skin scarring, IUGR |
Neonatal (around delivery) | Most common |
Neonatal forms | SEM / CNS / Disseminated |
Disseminated disease | Multi-organ failure, high mortality |
TABLE 11 — NEONATAL HSV RISK (NUMBERS TABLE)
Scenario | Risk |
Primary maternal HSV near delivery | 30–50% |
Recurrent HSV with lesions | 1–3% |
Asymptomatic shedding | Low but real |
📌 Exam logic: Primary near term = worst.
TABLE 12 — DIAGNOSIS IN PREGNANCY
Method | Role |
Clinical | Painful vesicles / ulcers |
PCR from lesion | Gold standard |
Viral culture | Older method |
HSV IgG serology | Primary vs recurrent |
Pregnancy approach | Clinical ± PCR |
TABLE 13 — ANTIVIRAL DRUGS (MECHANISM TABLE)
Aspect | Details |
Drug of choice | Acyclovir |
Prodrug | Valacyclovir |
Drug class | Guanosine analogue |
Activation | Viral thymidine kinase |
Active form | Acyclovir triphosphate |
Action | Inhibits viral DNA polymerase |
Effect | Chain termination |
Pregnancy safety | Safe |
Breastfeeding | Safe |
TABLE 14 — MANAGEMENT IN PREGNANCY (BIG PICTURE)
Question | Why |
Primary or recurrent? | Determines neonatal risk |
Gestation age | Near term = high risk |
Lesions at delivery? | Determines mode of delivery |
TABLE 15 — PRIMARY HSV MANAGEMENT IN PREGNANCY
Scenario | Management |
Any trimester | Oral acyclovir 400 mg TDS 5–10 days |
1st / 2nd trimester | Treat + reassure |
3rd trimester / <6 weeks to delivery | High risk |
Near term | Elective CS if lesions or recent infection |
≥36 weeks | Start suppressive therapy |
TABLE 16 — SUPPRESSIVE THERAPY (VERY HIGH-YIELD)
Aspect | Details |
Start | 36 weeks |
Drug | Acyclovir |
Dose | 400 mg TDS |
Alternative | Valacyclovir 500 mg BD |
Benefits | ↓ recurrences, ↓ shedding, ↓ CS |
TABLE 17 — DELIVERY DECISIONS
Situation | Mode of Delivery |
Primary HSV + lesions/prodrome | Caesarean |
Recurrent HSV + lesions | Usually CS |
No lesions or prodrome | Vaginal delivery OK |
SROM + primary HSV | Urgent CS |
SROM + recurrent HSV | CS usually offered |
TABLE 18 — POSTNATAL & BREASTFEEDING
Aspect | Guidance |
Breast milk | Virus not transmitted |
Breastfeeding | Allowed if no breast lesions |
Breast lesions | Avoid that side |
Kissing | Avoid if orolabial lesions |
Hygiene | Strict handwashing |
TABLE 19 — NEONATAL MANAGEMENT
Step | Action |
Assessment | Look for lesions |
Swabs | Mouth, NP, eye, rectum |
Tests | Blood ± CSF |
Empirical treatment | IV acyclovir |
Duration | 14–21 days |
TABLE 20 — SPECIAL HSV ENTITIES & COMPLICATIONS
Condition | Key Features |
Herpetic whitlow | Finger lesions, autoinoculation |
Eczema herpeticum | Painful monomorphic lesions on eczema |
Tzanck cells | Multinucleated giant cells |
Cowdry type A inclusions | Intranuclear inclusions |
Erythema multiforme | Immune-mediated |
Stevens–Johnson syndrome | Severe mucocutaneous reaction |
Sacral radiculopathy | Urinary retention, neural pain |
✅ This set is:
- Zero omission
- Exam-safe
- Viva-ready
- Table-only as requested
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