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Author Topic: Discovery of an endogenous Deltaretrovirus in the genome of bats (think Guanine)  (Read 46 times)

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A deltaretrovirus, rendered as a scientific cutaway illustration.

One important caveat: this is a conceptual illustration, not a verified structural model of a specific deltaretrovirus. The family/genus and genome labels in the generated image should not be treated as established taxonomy.

📝 Inline Markdownv4.6.5 · 2026-11-06

Claude: [November 14, 2026, 05:38:12 PM]

MINERVa — the missing deltaretrovirus fossil, found in bats

Farkašová et al., PNAS 114(12):3145–3150, 2017. Deltaretroviruses — the genus containing HTLV-1 and bovine leukemia virus — were the only retroviral genus with no known endogenous, germline-inherited fossil record. This paper closes that gap.

What they found

Screening mammalian genomes turned up a deltaretrovirus-like Gag sequence in the long-fingered bat Miniopterus natalensis, confirmed by PCR in four more Miniopterus species and named MINERVa. It's a 1,789-bp internal region between 604-bp LTRs, with a 6-bp target-site duplication, and it's strongly cytosine-rich — the deltaretroviral signature. Matrix and capsid proteins run 30.8% and 45.4% identity with HTLV-1, and it sits as a basal branch within the Deltaretrovirus clade.

Droplet digital PCR gave roughly one gag copy per haploid genome — a single insertion, orthologous across all five species, and absent from vespertilionids, cistugonids and more distant bats.

Age and dating caveat

The insertion predates the ~20 MYA Miniopterus radiation and is unlikely older than 45 MYA, giving a 45–20 MYA window. Notably, they couldn't use the standard LTR-divergence clock: some LTR pairs resemble each other more than their orthologs, and a 5-bp insertion shared by both LTRs in M. schreibersii points to gene conversion between them, which invalidates LTR-based dating.

Dead on arrival

Nearly everything from the end of gag through protease, polymerase and envelope is deleted — the authors suggest MINERVa was "dead on arrival," fixed in the germline already crippled, with no virus-driven copy-number amplification. The gag ORF survives intact in five of six alleles, but simulations reproduced that pattern 20% of the time, so there's no solid case for selection preserving it.

What's left is interesting though: ORF1 and ORF2 look like remnants of the 3′ accessory region — deltaretroviral nucleotide bias, a leucine-rich stretch resembling tax, a predicted Rex-responsive stem-loop, and overlapping ORFs mimicking the tax/rex arrangement. No detectable sequence homology to Tax or Rex, but those genes are poorly conserved anyway.

Why it matters

Deltaretroviruses have been infecting mammals for at least 20 million years, and their C-rich composition was already in place by the early Miocene. The paper extends the known host range to Chiroptera and completes the endogenous fossil record for all five mammalian retroviral genera. The authors float bat roosting and migration as transmission aids — though no current bat deltaretrovirus infection has been detected.

Weak points worth noting — one heavily deleted provirus means all inference about the ancestral virus is indirect; the dating rests on an assumed substitution rate and TimeTree estimates, and only nine non-miniopterid species were surveyed; the selection test looked at substitutions only, ignoring indels.

Sources: Discovery of an endogenous Deltaretrovirus in the genome of long-fingered bats

Oh yes, Hepatitis B (HBV) is a significant virus. But there's an interesting distinction: it's not necessarily dangerous in every person it infects, but its potential for long-term consequences is substantial.

And given our recent discussions about viral evolution, retroelements and genetic machinery, HBV is particularly interesting.

Why Hepatitis B matters

Diagram of Hepatitis B virus particle structure

  • Chronic infection: HBV can persist for decades, sometimes for life.

  • Liver damage: Persistent infection can cause chronic inflammation, fibrosis and cirrhosis.

  • Cancer: Chronic HBV infection is a major risk factor for hepatocellular carcinoma (liver cancer).

  • Immune evasion: HBV has sophisticated mechanisms for persisting despite immune surveillance.

  • Integration: HBV DNA can integrate into the host cell's genome. This is particularly interesting from an evolutionary and molecular biology perspective.

The really interesting molecular biology

HBV is not actually a retrovirus.

Feature               Hepatitis B                                 
Virus family           Hepadnaviridae                               
Genome                 Partially double-stranded DNA               
Replication           Reverse transcription                       
Enzyme                 Reverse transcriptase                       
Persistent intermediateNuclear cccDNA                               
Host genome integrationCan occur, but isn't required for replication

That reverse-transcription mechanism is fascinating: HBV makes an RNA intermediate and converts it back into DNA.

And importantly, its nuclear cccDNA can act as a persistent template for producing new viral components.

who.int +1

Just how big a deal?

240 million

People estimated to be living with chronic HBV globally in 2024.

Approximately 1.1 million deaths were attributed to HBV in 2024, predominantly through cirrhosis and liver cancer. who.int

One more connection to our previous discussion

There is also Hepatitis D (HDV).

Hepatitis Delta Virus: Replication Strategy and Upcoming Therapeutic Options for a Neglected Human Pathogen

HDV is particularly unusual because it depends on HBV to provide its envelope proteins. It has its own RNA genome and cannot establish infection without HBV.

That makes it a fascinating example of viral dependency and molecular cooperation.

Australian Centre for Disease Control +1

My take: HBV is an excellent organism to study if we're exploring the evolutionary relationship between RNA, DNA, reverse transcription, viral persistence and host genomes.

And one correction to our earlier illustration: Hepatitis D is not a deltaretrovirus either. The name is misleadingly similar.

I reckon there's plenty of evolutionary biology to explore here. 😁

« Last Edit: Yesterday at 02:56:14 PM by smfadmin »
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