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Quizzes > Science

Persistent viruses that can reactivate: practice quiz

Quick, free viral latency quiz to test your biology basics. Instant results.

Editorial: Review CompletedCreated By: Marcos BassilyUpdated Aug 23, 2025
Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art virus icons and test tubes arranged for microbiology quiz theme on golden yellow background.

This quiz helps you practice key ideas on persistent viruses that can reactivate periodically and the basics of viral latency. For more practice, try a quiz on viruses, compare pathways in a lytic vs lysogenic quiz, or see links with cancer in an oncogenic viruses quiz.

Which virus family includes herpes simplex virus type 1, known for latency in sensory neurons?
Retroviridae
Picornaviridae
Orthomyxoviridae
Herpesviridae
Herpes simplex virus type 1 (HSV-1) is a double-stranded DNA virus belonging to the Herpesviridae family, which is characterized by its ability to establish latency in sensory ganglia and periodically reactivate. Picornaviridae, Retroviridae, and Orthomyxoviridae are families of RNA viruses that cause distinct diseases but do not establish lifelong latency in neurons. Understanding the family classification helps in predicting viral behavior and treatment strategies.
What is viral latency?
A phase of antibody production
A stage of rapid viral replication
An acute infection leading to symptoms
A period where the virus persists in a dormant state in host cells
Viral latency refers to a phase in which the viral genome remains within host cells without producing infectious progeny, often evading immune detection. During this dormant state the virus can reactivate later under certain triggers. This is distinct from active infection when virus replication and symptoms occur.
In which cells does HSV-1 primarily establish latency after initial infection?
Lymphocytes
Epithelial cells
Sensory neurons
Hepatocytes
HSV-1 travels retrograde along sensory nerve axons to neuronal cell bodies, where it establishes a latent infection in sensory ganglia. Hepatocytes and lymphocytes are not reservoirs for HSV-1 latency, and epithelial cells support productive rather than latent infection. Recognizing the cellular reservoir is crucial for understanding reactivation pathways.
How does the herpesvirus genome typically persist in host cells during latency?
As linear RNA
Integrated into host chromosome
As free cytoplasmic DNA
As an episomal circular DNA in the nucleus
During latency, herpesvirus genomes exist as circularized episomes in the host cell nucleus, separate from host chromosomes, allowing them to persist without integration. This form avoids detection and maintains the viral genome in a stable state until reactivation. Integrated or free cytoplasmic forms are not characteristic of herpesvirus latency.
Which common trigger can lead to reactivation of latent herpesvirus?
Antibiotic treatment
Low blood sugar
Vaccination
Physical or emotional stress
Physical or emotional stress can induce physiological changes and weaken immune surveillance, promoting herpesvirus reactivation from latency. Antibiotics and vaccinations do not generally trigger viral reactivation, and low blood sugar is not a recognized factor. Stress management is often recommended to reduce outbreaks.
Varicella-zoster virus causes which primary infection before it becomes latent?
Mumps
Rubella
Measles
Chickenpox
Varicella-zoster virus (VZV) initially causes chickenpox, a widespread vesicular rash illness, before entering latency in sensory ganglia. Measles, rubella, and mumps are caused by other distinct viruses and do not lead to VZV latency. Recognizing the primary disease is key to understanding reactivation as shingles later in life.
After the primary infection, VZV remains latent in what location?
Liver
Dorsal root ganglia
Bone marrow
Lymph nodes
Following primary infection, VZV establishes latency in the dorsal root ganglia of the spinal nerve roots, where it can remain dormant for decades. Reactivation along the same sensory pathways leads to the characteristic dermatomal rash of shingles. The liver, bone marrow, and lymph nodes are not primary sites of VZV latency.
What is the function of latency-associated transcripts (LATs) during HSV-1 latency?
They encode viral capsid proteins
They help maintain viral latency by inhibiting lytic gene expression
They trigger host cell apoptosis
They integrate the viral genome
LATs are non-coding RNAs produced during HSV-1 latency that contribute to silencing lytic gene expression and protecting infected neurons from apoptosis. They do not code for structural proteins or integrate the viral genome. This regulatory function is essential for the establishment and maintenance of latency.
In which cell type does Epstein-Barr virus (EBV) typically establish latency?
Hepatocytes
B lymphocytes
T lymphocytes
Neurons
EBV primarily infects B cells and establishes latency in memory B lymphocytes, allowing it to evade immune detection and periodically reactivate. T lymphocytes, hepatocytes, and neurons are not the main reservoirs for EBV latency. Understanding EBV's tropism is important in diseases like mononucleosis and certain lymphomas.
Cytomegalovirus belongs to which herpesvirus subfamily?
Deltaherpesvirinae
Gammaherpesvirinae
Betaherpesvirinae
Alphaherpesvirinae
Human cytomegalovirus (HCMV) is classified within the Betaherpesvirinae subfamily, which is characterized by slow replication and the ability to establish latency in monocytes. Alphaherpesvirinae includes HSV and VZV, while Gammaherpesvirinae includes EBV and KSHV. No deltaherpesvirinae subfamily exists in human herpesviruses.
Which of the following DNA viruses is the most common cause of congenital infection and can reactivate in immunocompromised patients?
Parvovirus B19
Cytomegalovirus
Adenovirus
Human papillomavirus
CMV is the leading cause of congenital viral infection worldwide and can reactivate in immunocompromised hosts, leading to severe complications. Adenoviruses, Parvovirus B19, and HPV have different clinical implications and are not the primary congenital infection risk with reactivation potential in immune suppression.
What type of immune response is most important in controlling reactivation of latent herpesviruses?
Interferon-gamma alone
Complement activation
Cell-mediated immunity
Humoral immunity
T-cell - mediated immunity, particularly CD8+ cytotoxic T cells, plays a crucial role in surveilling and suppressing latent herpesviruses and preventing reactivation. Antibody-mediated (humoral) immunity contributes to limiting spread but is less effective in clearing latent reservoirs. Complement activation and isolated cytokine effects are supportive but not sufficient alone.
During viral reactivation, which class of herpesvirus genes is expressed first?
Late genes
Immediate early genes
Structural genes
Early genes
The reactivation cascade of herpesviruses begins with transcription of immediate early (IE) genes, which regulate subsequent expression of early and late genes required for viral replication. Early genes encode enzymes for DNA synthesis, while late genes encode structural proteins. Structural genes are not expressed until the late phase.
Which antiviral drug is commonly used to inhibit herpesvirus DNA polymerase during reactivation?
Acyclovir
Oseltamivir
Zidovudine
Ribavirin
Acyclovir is a guanosine analog that selectively inhibits herpesvirus DNA polymerase by chain termination during viral DNA synthesis, making it a first-line therapy for HSV and VZV reactivation. Oseltamivir targets influenza neuraminidase, ribavirin has broad RNA virus activity, and zidovudine is used against HIV reverse transcriptase.
What role do microRNAs from the HSV latency-associated transcript (LAT) play in latency?
They suppress expression of viral immediate early genes to maintain latency
They enhance viral capsid assembly
They integrate viral DNA
They induce host cell lysis
MicroRNAs derived from the HSV LAT region target and downregulate immediate early transcripts, reducing lytic gene expression and stabilizing the latent state. They do not promote capsid assembly or cause cytopathic effects. This post-transcriptional regulation is essential for long-term viral persistence.
During latent CMV infection, the virus is primarily harbored in which cell type?
Neurons
Epithelial cells
Monocytes and CD34+ hematopoietic progenitor cells
T cells
CMV establishes latency mainly in cells of the myeloid lineage, including monocytes and CD34+ progenitor cells in the bone marrow. Neurons are reservoirs for herpes simplex and VZV, not CMV. Epithelial cells and T cells support productive infection rather than long-term latency.
Which HSV glycoprotein binds complement component C3b to help evade the immune system?
Glycoprotein D
Glycoprotein B
Glycoprotein C
Glycoprotein H
HSV glycoprotein C (gC) can bind complement component C3b, blocking the formation of C3 convertase and limiting complement-mediated viral neutralization. Glycoproteins B, D, and H have other roles in viral entry and cell fusion but do not directly inhibit complement. Immune evasion by gC is a key factor in HSV pathogenicity.
In varicella-zoster virus latency, the viral genome remains in what form?
Linear RNA
Proviral RNA
Circular episomal DNA
Integrated DNA
During VZV latency, the circularized episomal form of viral DNA persists in the neuronal nucleus without integrating into host chromosomes. This allows the genome to remain transcriptionally silent except for latency-associated transcripts. No RNA or integrated forms define VZV persistence.
Which molecular technique is most sensitive for detecting latent viral genomes in tissue samples?
ELISA
Western blot
Polymerase chain reaction (PCR)
Hemagglutination assay
PCR is highly sensitive and specific for detecting small amounts of latent viral DNA in tissues, allowing amplification of target sequences. ELISA and Western blot detect proteins or antibodies, not latent genomes, while hemagglutination assays measure viral particle binding. PCR remains the gold standard for genome detection.
A Tzanck smear is used diagnostically to identify which virus?
Cytomegalovirus
Epstein-Barr virus
Varicella-zoster virus
Herpes simplex virus
A Tzanck smear reveals multinucleated giant cells formed by membrane fusion in cells infected with HSV. While VZV can also produce similar cytopathic effects, the technique is most commonly used for HSV diagnosis in clinical settings. CMV and EBV do not typically produce giant cells on Tzanck smear.
Which host cell organelle stress response is implicated in triggering herpesvirus reactivation?
Peroxisomal proliferation
Endoplasmic reticulum stress
Mitochondrial unfolded protein response
Golgi fragmentation
Endoplasmic reticulum (ER) stress can activate cellular signaling pathways such as the unfolded protein response, which has been linked to reactivation of latent herpesviruses. Mitochondrial or peroxisomal stress and Golgi changes are less directly associated with viral reactivation. Managing ER stress can thus influence latency.
Which viral transcript is typically limited to latency and not expressed during lytic infection in HSV?
DNA polymerase transcript
gB mRNA
Latency-associated transcript (LAT)
ICP0
The LAT is the only abundant viral transcript during HSV latency and plays a role in silencing lytic gene expression. ICP0, glycoprotein B (gB), and DNA polymerase are expressed during active lytic replication and not during latency. This distinction is key for diagnosing latent infections.
What epigenetic modification is commonly found on latent HSV chromatin to maintain gene silencing?
Histone H4 acetylation
DNA adenine methylation
Histone phosphorylation
Histone H3 lysine 9 trimethylation (H3K9me3)
Latency of HSV is associated with heterochromatin formation at lytic gene promoters, marked by H3K9me3, leading to transcriptional repression. Histone acetylation and phosphorylation are typically linked to active transcription, and DNA adenine methylation is not a major mechanism in mammalian latent herpesviruses. Epigenetic control is crucial for maintaining latency.
Which EBV-encoded microRNA is known to target viral immediate early transcripts to promote latency?
miR-BART2
miR-21
miR-155
miR-122
EBV miR-BART2 targets the viral DNA polymerase mRNA (BALF5), reducing lytic replication and reinforcing latency. miR-155, miR-21, and miR-122 are host or other viral miRNAs involved in different regulatory pathways but do not directly maintain EBV latency. These virus-encoded miRNAs fine-tune the switch between latency and lytic phases.
Which antiviral drug specifically targets the CMV terminase complex to prevent CMV reactivation in transplant patients?
Foscarnet
Ganciclovir
Valacyclovir
Letermovir
Letermovir inhibits the CMV terminase complex, blocking viral DNA cleavage and packaging without affecting DNA polymerase, and is approved for CMV prophylaxis in hematopoietic stem cell transplant patients. Valacyclovir and ganciclovir target viral DNA polymerase, while foscarnet also inhibits polymerase but with more toxicity. Letermovir's specific mechanism reduces reactivation risk.
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Study Outcomes

  1. Identify Persistent Viruses That Reactivate Periodically -

    Explain what persistent viruses that can reactivate periodically are and how they maintain latency and trigger recurrent infections in host cells.

  2. Analyze Host Dependence of Viral Replication -

    Describe why viruses are unable to multiply outside of a host cell by examining viral replication mechanisms and host-cell interactions.

  3. Classify Major Virus Families -

    Differentiate between virus family names - such as Herpesviridae and Orthomyxoviridae - based on defining genomic and structural characteristics.

  4. Differentiate Oncogenic from Non-Oncogenic Viruses -

    Apply "oncogenic viruses include all the following except" scenarios to identify which viruses are truly associated with tumor formation versus those that are not.

  5. Explain Naked RNA Viral Structures -

    Explain what naked strands of RNA not covered by a capsid are and assess their impact on viral stability and classification.

Cheat Sheet

  1. Mechanisms of Viral Latency -

    Persistent viruses that can reactivate periodically are often members of the Herpesviridae family, such as HSV-1 and VZV, which establish latency in neurons. Reactivation triggers include stress, UV exposure, and immunosuppression. Mnemonic "HERePAWs" helps recall: Herpes Entering Nerve cells, Pause, Awakening by Stress.

  2. Virus Family Nomenclature -

    Identifying which of the following represents a virus family name hinges on the suffix "-viridae," like Picornaviridae or Togaviridae. Remember "Viridae = Very Important Reliable Infectious Disease Entities Always" to spot true family names. This systematic naming comes from the International Committee on Taxonomy of Viruses (ICTV).

  3. Obligate Intracellular Replication -

    Viruses are unable to multiply outside of a host cell because they lack critical organelles such as ribosomes and mitochondria for ATP production. They hijack host machinery for transcription and translation, making them obligate intracellular parasites. Recall the phrase "no host, no growth" to cement this concept.

  4. Oncogenic Virus Exceptions -

    Oncogenic viruses include all the following except Rhinovirus; key oncogenic families are Papillomaviridae (HPV), Hepadnaviridae (HBV), and Herpesviridae (EBV). Use the mnemonic "H³: HPV, HBV, HHV-4 (EBV)" to remember true oncogenic agents. This classification is supported by WHO and CDC cancer studies.

  5. Naked RNA Agents: Viroids -

    Naked strands of RNA not covered by a capsid are known as viroids, which are small, circular, plant-infecting molecules. Unlike viruses, viroids lack a protein coat and rely on host RNA polymerases for replication. A classic example is the Potato Spindle Tuber Viroid, best remembered by "PSTV causes tuber twists."

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