A mathematical model that combines stochasticity and spatial structure describes the dynamics of the viral population during an infection cycle, and fitting the model to RNA and virus abundances over time shows that poliovirus follows a geometric replication mode.

An individual-based model framework of sub-exponentially growing replicator systems suggests that parabolic dynamics could have been able to maintain genetic diversity and circumvent the error threshold problem during early evolution.

Cryo-electron tomography unveils striking new structural components of positive-strand virus RNA replication compartments, greatly advancing mechanistic insights into the structure, assembly, function and control of these critical complexes.

All steps of a viroid-like replication cycle can be catalyzed by RNA alone.

A cytorhabdovirus phosphoprotein hijacks host CCR4 to trigger turnover of viral nucleoprotein (N)-bound cellular RNAs, thereby releasing nascent RNA-free N protein molecules to bind viral genomic RNAs for optimal replication.

Human proteins that add or remove the methyladenosine modification of cellular RNA, or recognize methylated RNA significantly affect HIV-1 infection or viral protein synthesis in cells, suggesting an important role for HIV-1 RNA methylation in regulating viral replication.

In an in vitro RNA replication system, an RNA spontaneously diversifies and continuously evolves through coevolution with parasitic entities.

SND1 has m6A-reading ability and is essential for Kaposi's sarcoma-associated lytic replication.

Replication origins are established throughout the genome with the exception of transcribed genes, and the local chromatin composition likely modulates the density of ORC and MCM as well as origin activation.

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.