https://www.sciencedirect.com/science/article/pii/S1071909125000348?via%3Dihub
- Tämån vuoden artikkelista olennaista tietoa CHIKV viruksesta ja vektorista.
- LÄHDETIEDOT:
Seminars in Pediatric Neurology
Volume 54, July 2025, 101213Chikungunya virus infection: A scoping review highlighting pediatric systemic and neurologic complications
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Epidemiology
Aedes
aegypti and Aedes albopictus are the primary vectors responsible for
the transmission of several medically significant arboviruses, including
dengue, Zika, yellow fever, and chikungunya viruses.4
Aedes aegypti, originally native to Africa, has expanded globally via
maritime trade and now predominantly inhabits tropical and subtropical
urban regions. It demonstrates endophilic behavior and a strong
preference for human hosts, contributing to its high vectorial capacity
in densely populated areas.5,6
In contrast, Aedes albopictus, native to Asia, has successfully
colonized both tropical and temperate climates.
Its ability to produce
cold-resistant diapausing eggs enables overwintering in cooler Environmental temperature plays a critical role in modulating CHIKV
transmission. Higher temperatures have been shown to accelerate viral
replication within the mosquito and reduce the extrinsic incubation
period, thereby enhancing infectivity.12,13
Consequently, climate change may facilitate the expansion of Aedes
vectors into regions previously unsuitable for sustained transmission.
This phenomenon has already manifested in parts of Europe, where local
cases of CHIKV and other arboviral infections have recently
Chikungunya
virus (CHIKV) is an enveloped, single-stranded, positive-sense RNA
virus belonging to the Alphavirus genus within the Togaviridae family.
Its envelope glycoproteins (gp.) , E1 and E2, form heterodimers that organize
into trimeric spikes on the virion surface, mediating host cell entry.
E1 contains a hydrophobic fusion peptide crucial for membrane fusion,
while E2 facilitates receptor binding and is the principal target of
host neutralizing antibodies. During maturation, the precursor protein
p62—comprising E2 and E3—is processed in the trans-Golgi network (TGN), with
E3 remaining associated with E2 until final virion assembly is complete.
CHIKV engages host cell receptors including glycosaminoglycans (gag) and the
adhesion molecule Mxra8, which promotes viral attachment and
internalization. Entry is predominantly mediated by clathrin-dependent
endocytosis and macropinocytosis, both of which require endosomal
acidification.17,18
emerged.14, 15, 16 environments, facilitating its global spread since the 1960s.6,7In addition to viral and host factors, the mosquito’s microbiota
significantly influences CHIKV replication and transmission. The gut
microbiome can alter virus dynamics following a blood meal19 and modulate the vector's innate immune response.20
Among the microbial inhabitants, Wolbachia—an intracellular, maternally
transmitted bacterium present in approximately 60 % of insect
species—has emerged as a potential tool for vector control. While Aedes
albopictus naturally harbors Wolbachia, Aedes aegypti does not.21
However, experimental introduction of Wolbachia into A. aegypti has
been shown to suppress CHIKV replication, likely through immune priming
mechanisms.21,22
Clinical manifestations
Chikungunya
virus (CHIKV) is associated with high attack rates during outbreaks
(35–75 %), such as during the Réunion Island epidemic, where
laboratory-confirmed cases totaled 16,050 and estimated cases reached
244,000 (35 % attack rate).28,29
CHIKV infection presents age-dependent clinical features and severity,
ranging from mild febrile illness in children to severe multisystem
disease in neonates and chronic sequelae in adults. Recognizing these
patterns is essential to guide diagnosis, monitoring, and management.
Systemic manifestations
Overall,
systemic chikungunya presents a spectrum of disease severity. While
adults bear the brunt of chronic rheumatologic sequelae, neonates face
the most acute risk of life-threatening complications, and children
typically experience intermediate, self-limited illness with some risk
of complications in infancy.
Neonates
They are at the highest risk for severe systemic disease, especially those born to viremic mother
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