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2017 ; 8
(ä): 567
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Serum Cytokine Profiles Differentiating Hemorrhagic Fever with Renal Syndrome and
Hantavirus Pulmonary Syndrome
#MMPMID28572804
Khaiboullina SF
; Levis S
; Morzunov SP
; Martynova EV
; Anokhin VA
; Gusev OA
; St Jeor SC
; Lombardi VC
; Rizvanov AA
Front Immunol
2017[]; 8
(ä): 567
PMID28572804
show ga
Hantavirus infection is an acute zoonosis that clinically manifests in two
primary forms, hemorrhagic fever with renal syndrome (HFRS) and hantavirus
pulmonary syndrome (HPS). HFRS is endemic in Europe and Russia, where the mild
form of the disease is prevalent in the Tatarstan region. HPS is endemic in
Argentina, as well as other countries of North and South American. HFRS and HPS
are usually acquired via the upper respiratory tract by inhalation of
virus-contaminated aerosol. Although the pathogenesis of HFRS and HPS remains
largely unknown, postmortem tissue studies have identified endothelial cells as
the primary target of infection. Importantly, cell damage due to virus
replication, or subsequent tissue repair, has not been documented. Since no
single factor has been identified that explains the complexity of HFRS or HPS
pathogenesis, it has been suggested that a cytokine storm may play a crucial role
in the manifestation of both diseases. In order to identify potential serological
markers that distinguish HFRS and HPS, serum samples collected during early and
late phases of the disease were analyzed for 48 analytes using multiplex magnetic
bead-based assays. Overall, serum cytokine profiles associated with HPS revealed
a more pro-inflammatory milieu as compared to HFRS. Furthermore, HPS was strictly
characterized by the upregulation of cytokine levels, in contrast to HFRS where
cases were distinguished by a dichotomy in serum cytokine levels. The severe form
of hantavirus zoonosis, HPS, was characterized by the upregulation of a higher
number of cytokines than HFRS (40 vs 21). In general, our analysis indicates
that, although HPS and HFRS share many characteristic features, there are
distinct cytokine profiles for these diseases. These profiles suggest a strong
activation of an innate immune and inflammatory responses are associated with
HPS, relative to HFRS, as well as a robust activation of Th1-type immune
responses. Finally, the results of our analysis suggest that serum cytokines
profiles of HPS and HFRS cases are consistent with the presence of extracellular
matrix degradation, increased mononuclear leukocyte proliferation, and
transendothelial migration.