Since 1972 the WHO (the UN) called for/recommended virologists develop the means to prolong virus/coronavirus infections by impairing immune response to a virus:
The below screenshot was taken from the Bulletin of the World Health Organization, Volume 47, p.259, 1972, Recommendations (3)
Virologists prolonged virus/coronavirus infections for the WHO by genetically engineering/modifying the SARS coronavirus in 2003. The human herpes virus protein ORF10 was encoded into the SARS coronavirus to make the novel SARS-CoV-2 – created in 2003 patent US-2006257852-A1
The patent was abandoned because the WHO intended on using it as a biological weapon. AIDS was caused by the WHO using smallpox vaccines made with the live viral component of the infectious and deadly vaccinia virus.
AIDS is now treatable so the WHO needed a new virus to make $billions in treating, not curing, the novel disease. The herpes virus ORF10 protein was intentionally encoded in SARS to cause and prolong SARS-CoV-2 infections.
“These results indicate that ORF10, like its HSV-1 homolog VP16, is a transactivating protein despite the absence of sequences similar to the VP16 carboxy-terminal domain. The transactivating function of the ORF10 tegument protein may be critical for efficient initiation of viral infection” 1993 Journal of Virology published study
In the context of gene regulation: transactivation is the increased rate of gene expression triggered either by biological processes or by artificial means, through the expression of an intermediate transactivator protein. HIV, HTLV and 2003 patented SARS-CoV-2 are three of the many viruses that encode transactivating proteins (e.g. ORF10) to enhance viral gene expression.
“Viral mRNA can efficiently hijack host ribosomes during infection for translation of proteins necessary for virus propagation. Initiation of translation is a key step, during which the coding region of mRNA, open reading frame (ORF), gets properly positioned on the ribosome.” UMass Medical School
“Nuclear export of host mRNAs is critical for proper cellular functions and survival. To mitigate this effort, viruses have evolved multiple strategies to inhibit this process. Distinct to the generally nonselective inhibition mechanisms, ORF10 from gammaherpesviruses blocks nuclear export of selective mRNAs by forming a complex with Rae1 (RNA export 1) and Nup98 (nucleoporin 98).” October 8, 2020 published research article – Molecular mechanism underlying selective inhibition of mRNA nuclear export by herpesvirus protein ORF10