Figure legends:
Figure 1: Structure of SARS-CoV-2 Virus with its typical capsid and the
spikes, “corona”.
ssRNA=single stranded RNA; ACE2=Angiotensin receptor 2;
TMPRSS2=transmembrane protease serine subtype 2.
Figure 2: Symptoms of COVID-19.
Figure 3: Cascade of events in lung epithelium during SARS-CoV-2
infection. SARS-CoV-2 infects lung epithelial cells via ACE2 and TMPRSS2
receptor, the host cells undergo apoptosis in consequence of virus
replication and release and the undergoing cell releases
damage-associated molecular patterns, which induce the production of
pro-inflammatory mediators by epithel and endothel cells in the
neighbourhood. Inflammatory cells such as monocytes, macrophages, and T
cells are recruited from the blood to the lung epithel, increase the
production of inflammatory mediates and further infiltration of the lung
by inflammatory cells, leading to damage of the lung structure and a
“cytokine storm”, which reaches the vasculature and other organs.
ssRNA=single stranded RNA; ACE2=Angiotensin receptor 2;
TMPRSS2=transmembrane protease serine subtype 2; Mo=monocyte, T=T
lymphocyte, M=macrophage.
Figure 4 A: Typical skin lesions (vesicular eruptions occurring early
during COVID-19 (A), with symptoms of COVID-19, i.e. maculopapular
exanthema (B), urticarial rash (C), vasculitis (D) and later during
COVID-19 disease Chilblain eruptions (E).
Figure 5: Immunologic features in the skin of virus-induced
maculopapular exanthema (A) with virus antibody activation and
interaction with immune cells in the blood, recruitment of activated
cells to the skin, extravasation of erythrocytes through the blood
vessels,, cytokine production and keratinocyte apoptosis and related
changes to the dermis and epidermis and drug-induced maculopapular rush
type IVb (B) and IVc (C) derived by activated T cells, extravasation of
erythrocytes, perivascular infiltrates and perforin and granzyme B and
Th1 cytokines as well as different chemokines and recruitment of T cells
and eosinophils to the dermis and respective changes to the dermis and
epidermis; DC=dendritic cell; B=B cell; Mo=monocyte, Eo=Eosinophil.
Figure 6: Histologic features of skin biopsies taken from two SARS-CoV-2
positive patients with maculo-papular eruptions.
A: Skin sections showing epidermis with mild hyperkeratosis,
keratinocytes with frosted glass nuclei, with intranulcular and
occasionally multinucleate inclusions,
reminiscent of cytopathic damage. Dermis without edema, perivascular
inflammatory infiltrate extending focally to the basal layer, causing
slight vacuolate damage and
pigmentary incontinence. No eosnophils are observed
B: Histology (H&E stain) showing an inconspicous epdermis and a very
subtle perivascular lymphohistiocytic infiltrate in the upper dermis
with admixture of few eosinophilic granulocytes.
Figure 7: IgE-, direct- and antigen-immuncomplex-mediated mast cell
activation in urticaria.
Figure 8: Vasculitis of small, medium and large vessels, with formation
of antigen-immune-complexes, which accumulate within the vessels and
damage of the endothel, which leads to extravasation of cells and
neutrophil recruitment.
Figure 9 A: 58-year old male patient diagnosed with COVID-19 and DRESS
syndrome.
B: Histology (H&E stain) showing interface changes (vacuolar
degeneration of the basal layer, apoptotic keratinocytes, exocytosis of
lymphocytes) as well as spongiotic changes with hyperparakeratosis.
Perivascular lymphohistiocytic infiltrate with admixture of few
eosinophilic granulocytes. Mild extravasation of erythrocytes.