The attachment of PBCV-1 to its receptor is very specific, and a major source of limitation with regards to viral host range. Virus-associated enzymes allow the host cell wall to degrade, and the viral internal membrane fuses with the host membrane. This fusion allows the transfer of viral DNA and virion-associated proteins into the host cell and also triggers depolarization of the host membrane. This is presumably occurring due to a virus encoded K+ channel. Studies predict this channel is within the virus, acting as an internal membrane releasing K+ from the cell, which may assist in the ejection of viral DNA and proteins from the viral cell to its host. The depolarization of the host’s cell membrane is also thought to prevent secondary infection from another virus or secondary transporters. Because PBCV-1 does not have an RNA polymerase gene, its DNA and viral-associated proteins move to the nucleus where transcription begins 5–10 minutes post infection. This rapid transcription is attributed to some component facilitating this transfer or viral DNA to the nucleus. This component is assumed to be a product of the "PBCV-a443r" gene, which obtains structures resembling proteins involved in nuclear trafficking in mammalian cells. Host transcription rates decrease in this early phase of infection, and host transcription facilitators are reprogrammed to transcribe the new viral DNA. Minutes after infection, host chromosomal DNA degradation begins. This is presumed to occur through PBCV-1 encoded and packaged DNA restriction endonucleases. Degradation of the host chromosomal DNA inhibits host transcription. This results in 33-55% of the polyadenylated mRNAs in the infected cell being of viral origin by 20 minutes after initial infection. Viral DNA replication initiates after 60 to 90 minutes, which is then followed by the transcription of late genes within the host cell. Roughly 2–3 hours post infection, the assembly of virus capsids begins. This occurs within localized regions of the cytoplasm, with the virus capsids becoming prominent 3–4 hours after initial infection. 5–6 hours after PBCV-1 infection, the cytoplasm of the host cell fills with infectious progeny virus particles. Shortly after that (6–8 hours post infection), localized lysis of the host cell releases progeny. ~1000 particles are released from each infected cell, ~30% of which form plaques. In algae infected with Cloroviruses the result is lysis, and thus death.