Dengue virus — Questions

Expanded dengue syndrome describes organ-specific disease, such as hepatitis, myocarditis or encephalopathy, beyond the classical plasma-leakage picture.

Dengue is not chronic, the term is not a vaccine effect, and it is neither limited to pregnancy nor a description of Zika co-infection.

Infection gives durable protection against the infecting serotype but only short-lived cross-protection against the other three, which is why a later heterologous infection is possible and dangerous.

Immunity is neither lifelong across all serotypes nor absent, and it is not limited to a single other serotype or sterilising for the genus.

Qdenga can be given without screening a recipient’s dengue serostatus first, and is WHO-recommended for children in high-transmission settings.

It still needs a cold chain and two doses, protects only against dengue, and does not replace vector control.

Infection near delivery can cause neonatal dengue and raises the risk of preterm birth, low birth weight and peripartum haemorrhage.

There is a real perinatal risk, and the congenital defects listed belong to rubella and varicella, not dengue.

Host furin cleaves prM in the trans-Golgi network as the particle exits, priming it for infectivity; incomplete cleavage leaves a mixture of mature and immature virions.

NS3 processes the polyprotein, not prM at maturation, and neuraminidase, caspases and host RNA polymerase have no role here.

Dengue is a positive-sense RNA flavivirus (genus Orthoflavivirus) with four serotypes, DENV-1 to DENV-4.

It is not segmented or negative-sense, not a DNA virus or retrovirus, and not an alphavirus (the arthritogenic Togaviridae).

The critical phase begins around defervescence, typically days 4 to 6, which is why a settling fever can dangerously masquerade as improvement.

Leakage is not a feature of the first febrile day, the incubation period or the recovery phase, and it does not wait three weeks.

Memory T cells raised against the first serotype respond poorly to the second and release a disproportionate cytokine burst, a T-cell “original antigenic sin” that helps drive the vascular leak.

They do not clear the virus faster, make sterilising antibody, prevent viraemia or block Fc receptors.

In the first few days the virus is detected directly, so NS1 antigen and RT-PCR are the tests of choice; RT-PCR also gives the serotype.

Serology is unreliable this early, blood culture does not grow the virus, and the tourniquet test supports assessment but does not confirm the diagnosis.

No dengue vaccine is positioned as a routine measure for the general traveller. Dengvaxia is used only in proven previously-infected residents of endemic areas, and although Qdenga is prequalified and widely used in endemic programmes, it is not a standard traveller vaccine.

Bite avoidance remains the mainstay for travellers, and no dengue vaccine is an entry requirement.

NS1 is secreted from infected cells and circulates in the blood, giving an early antigen test in the first few days of illness; it also contributes to the endothelial leak.

The envelope protein is the neutralising target, the capsid protein forms the capsid, NS5 is the polymerase, and the envelope protein mediates receptor binding.

Dengvaxia is restricted to people with confirmed prior dengue infection, because in dengue-naive recipients it behaves like a first infection and primes for severe disease.

It is therefore not for the dengue-naive, and age and pregnancy are not the defining restriction.

Severe dengue is most associated with a second infection by a different serotype, through antibody-dependent enhancement, in which non-neutralising antibody from the first infection helps the second virus enter cells.

This is why priming a dengue-naive person with vaccine can be hazardous; the other options do not raise the risk.

Aedes aegypti, a day-biting, container-breeding mosquito adapted to human dwellings, is the principal urban vector, with Aedes albopictus secondary.

Culex transmits West Nile and Japanese encephalitis, Anopheles transmits malaria, and the ticks listed transmit tick-borne, not mosquito-borne, viruses.

A second infection with a different serotype is the single greatest risk factor for severe dengue, acting through antibody-dependent enhancement.

A first infection, malaria co-infection, prior flavivirus vaccination and sex are not the principal drivers, though infants of immune mothers are a related special case.

The urban cycle is a human-to-human loop transmitted by Aedes aegypti, distinct from the sylvatic (jungle) cycle that maintains these viruses among forest animals and forest mosquitoes. Anopheles transmits malaria, and Ixodes is a tick.

Meticulous fluid balance through the critical phase, with avoidance of non-steroidal anti-inflammatory drugs, is the core of management; paracetamol is preferred for fever.

Platelets are transfused for bleeding rather than a number alone, aspirin worsens bleeding, corticosteroids do not help, and there is no specific antiviral.

Persistent vomiting and abdominal pain are recognised warning signs, alongside mucosal bleeding, lethargy, fluid accumulation and a rising haematocrit with falling platelets.

Fever, headache and myalgia are features of uncomplicated dengue, and an isolated loose stool is not a warning sign.