(DKA) at onset, earlier-treatment initiation that can potentially pro-
long remission phase (reducing the risk of chronic complications in
future), and opportunity to take part in studies aiming at slowing/
stopping the progression to stage 3. It is unknown whether an earlier
diagnosis of T1D, at stage 1 or 2, may lead to earlier diabetes burnout.
Hence, psychological stress related to being autoantibody-positive
and waiting for progression when having no approved and widely
available treatment possibility should also be considered. Another
important topic related to T1D screening is the management and care
for the whole new group of patients. We are required to develop edu-
cational approaches and programs, psychological support, screening
tools (burden, burnout, and stress), care, and treatment options specif-
ically for stages 1 and 2, which differ a great deal from clinically symp-
tomatic T1D. These will be very interesting directions for developing
new research projects.
long remission phase (reducing the risk of chronic complications in
future), and opportunity to take part in studies aiming at slowing/
stopping the progression to stage 3. It is unknown whether an earlier
diagnosis of T1D, at stage 1 or 2, may lead to earlier diabetes burnout.
Hence, psychological stress related to being autoantibody-positive
and waiting for progression when having no approved and widely
available treatment possibility should also be considered. Another
important topic related to T1D screening is the management and care
for the whole new group of patients. We are required to develop edu-
cational approaches and programs, psychological support, screening
tools (burden, burnout, and stress), care, and treatment options specif-
ically for stages 1 and 2, which differ a great deal from clinically symp-
tomatic T1D. These will be very interesting directions for developing
new research projects.
LOOKING DEEPER INTO PANCREAS IN
TYPE 1 DIABETES (PRESENTED BY LARS
KROGVOLD)
TYPE 1 DIABETES (PRESENTED BY LARS
KROGVOLD)
The association between viral infection and T1D has been suggested
by epidemiological studies, but the direct proof is still missing. The
DiViD study investigated the underlying cause and mechanism of the
disease process by collecting pancreatic tissue, using a minimal laparo-
scopic pancreatic tail resection, from live adult patients with newly
diagnosed T1D.4 Although the study was terminated by the sixth
patient, it provided evidence for 30 peer-reviewed articles and several
by epidemiological studies, but the direct proof is still missing. The
DiViD study investigated the underlying cause and mechanism of the
disease process by collecting pancreatic tissue, using a minimal laparo-
scopic pancreatic tail resection, from live adult patients with newly
diagnosed T1D.4 Although the study was terminated by the sixth
patient, it provided evidence for 30 peer-reviewed articles and several
PhD-thesis in different countries and can be shown as an example for
extensive international collaborations.
extensive international collaborations.
The material allowed to study
insulin secretion by the islets after glucose perfusion, T-cell infiltration,
as well as presence of viruses, virus mediated responses and inter-
ferons. The enterovirus genome was detected in the pancreas of all the
DiViD participants and isolated viruses were found infective for new
cell cultures. The noted gene expression suggested a role for viral infec-
tion at this stage of the disease process.5 As a result, a prospective, ran-
domized, double-blinded, placebo-controlled intervention study was
started in Oslo, Norway and Copenhagen, Denmark. A total of 96 newly
diagnosed children aged 6–15 years were recruited till 2020, received
antiviral treatment–Pleconaril, Ribavirin–or placebo for 6 months and
are currently closely followed for 3 years to study the change their
mean residual insulin secretion and multiple other secondary endpoints.
The outcomes are awaited with great interest because an intervention
that minimizes viral infection may be effective in slowing the rate of
progression even in presymptomatic individuals.
insulin secretion by the islets after glucose perfusion, T-cell infiltration,
as well as presence of viruses, virus mediated responses and inter-
ferons. The enterovirus genome was detected in the pancreas of all the
DiViD participants and isolated viruses were found infective for new
cell cultures. The noted gene expression suggested a role for viral infec-
tion at this stage of the disease process.5 As a result, a prospective, ran-
domized, double-blinded, placebo-controlled intervention study was
started in Oslo, Norway and Copenhagen, Denmark. A total of 96 newly
diagnosed children aged 6–15 years were recruited till 2020, received
antiviral treatment–Pleconaril, Ribavirin–or placebo for 6 months and
are currently closely followed for 3 years to study the change their
mean residual insulin secretion and multiple other secondary endpoints.
The outcomes are awaited with great interest because an intervention
that minimizes viral infection may be effective in slowing the rate of
progression even in presymptomatic individuals.
HUMAN GUT MICROBIOME OR ARE
THE VIRUSES IN THE STOOL THE KEY?
(PRESENTED BY ONDREJ CINEK)
THE VIRUSES IN THE STOOL THE KEY?
(PRESENTED BY ONDREJ CINEK)
Viruses of intestinal origin have been long suspected of triggering the
islet autoimmunity or accelerating it towards the progression to symp-
tomatic T1D. Molecular studies of candidates among human gut
viruses performed so far have led to identification of important asso-
ciation signals with islet autoimmunity or T1D. As candidates for
islet autoimmunity or accelerating it towards the progression to symp-
tomatic T1D. Molecular studies of candidates among human gut
viruses performed so far have led to identification of important asso-
ciation signals with islet autoimmunity or T1D. As candidates for
involvement in T1D etiology enterovirus, rotavirus, SARS-Cov-2, and
human endogenous retroviruses are extensively investigated.
human endogenous retroviruses are extensively investigated.
Molecular tests revealed enterovirus presence at initiation of islet autoimmu-
nity and disease progression.6 Several studies have been published on
intestinal viromes and presymptomatic T1D, but no statistically signifi-
cant association was detected with known viruses.7 Epidemiological
data suggest a coincidence of rotavirus infection and the decrease of
celiac disease, but also–to a minor extent–T1D incidence.8 However,
results on the relation between rotavirus and T1D are inconclusive.9
What might the future bring? Further observation of the out-
comes of rotavirus vaccination carried out for other reasons than dia-
betes. The vaccination against Coxsackievirus B group–now being
nity and disease progression.6 Several studies have been published on
intestinal viromes and presymptomatic T1D, but no statistically signifi-
cant association was detected with known viruses.7 Epidemiological
data suggest a coincidence of rotavirus infection and the decrease of
celiac disease, but also–to a minor extent–T1D incidence.8 However,
results on the relation between rotavirus and T1D are inconclusive.9
What might the future bring? Further observation of the out-
comes of rotavirus vaccination carried out for other reasons than dia-
betes. The vaccination against Coxsackievirus B group–now being
tested. The ongoing research focused on microbial diversity.10
