Background and aims: Interferon-alpha plays a key role in
neurocognitive defects associated with human
immunodeficiency virus (HIV) and HIV encephalitis. The
aim of this study was to assess the effects of a novel
inhibitor of interferon-alpha (B18R) in an HIV encephalitis
severe combined immunodeficiency mouse model.
Methods: Human macrophages were cultured and infected
with HIV-1. Mice (5 week old B6.CB17-Prkdcscid/SzJ)
were inoculated with HIV-infected (n=16) or uninfected
(n=8) macrophages. The B18R was produced by a modified
recombinant procedure. Each B18R treated mouse received
50 mcg per day for 10 days. Brain sections were stained by
an immunoperoxidase method. The genes ISG15, IFNA4,
and Ifrg15 were analyzed using real-time polymerase chain
reaction (PCR).
Results: Gene expression of interferon-alpha signaling was
downregulated in the brain by B18R as shown by
polymerase chain reaction (PCR). Mononuclear phagocytes
were significantly decreased in mice treated with B18R
when compared to untreated mice. However, neuronal
arborizations were significantly retained in mice treated
with B18R when compared to untreated mice. Significant
increase in mononuclear phagocytes and loss of neuronal
arborization are prominent signs of HIV encephalitis.
Findings of this study indicated that the B18R crossed the
blood-brain barrier, blocked interferon-alpha signaling in
the brain, and improved defects associated with HIV
encephalitis.
Conclusion: Findings of this study might suggest that
B18R is a potential alternative to monoclonal antibodies
used in the management of HIV encephalitis. Further
studies are still needed to fully elucidate the effects of B18R
in HIV encephalitis.

عنوان المؤتمر

The 6th Congress of the European Academy of Neurology

دولة المؤتمر

فرنسا

تاريخ المؤتمر

22 مايو، 2020 - 24 مايو، 2020

راعي المؤتمر

European Academy of Neurology

معلومات إضافية

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