An increased emphasis on falsification – the direct testing of strong hypotheses – will lead to faster progress in science by allowing well-specified hypotheses to be eliminated.

Host restriction factors that block cross-species transmission also play a role in limiting the replication of highly-adapted HIV-1 in IFN-stimulated cells.

CRISPR genome editing technology can efficiently introduce mutations into lytic and latent HSV genomes to block lytic replication and reactivation of latent herpes simplex virus genome though differential mechanisms.

The initiation of human genome replication requires the six-subunit origin recognition complex (ORC) and CDC6, with ORC playing additional roles during mitosis and in organization of the cell nucleus.

TRF1 suppresses replication fork stalling, which triggers break induced replication at telomeres associated with DNA damage response, alteration in the telomere chromatin environment, and re-localisation of telomeres to PML bodies.

Rudimentary cross-catalytic replication can be established by double-hairpins of tRNA-like sequences, implying that replication and translation could have emerged along a common evolutionary trajectory.

Publication bias, in which positive results are preferentially reported by authors and published by journals, can restrict the visibility of evidence against false claims and allow such claims to be canonized inappropriately as facts.

Horizontal transfer of a sequence-specific DNA-binding domain allows a virus to destroy its subviral parasite and overcome parasite-mediated restriction.

A key cellular stress granule protein, G3BP1, is critical for efficient norovirus infection, representing the first pan-norovirus, pro-viral factor identified to date.

Empirical evaluations demonstrate the low probability of finding and replicating significant associations between psychological tests and brain structure in healthy adults, highlighting the importance out-of-sample replication of exploratory findings.